Вінницький національний медичний університет ім. М.І. …
Chapter 7
Diseases of periodontal tissues
Inflammatory and inflammatory-dystrophic diseases of periodontium.
“Periodontology” is the specialty that studies the tooth-supporting tissues - “periodontium”. The periodontium is made up of those tissues that surround each tooth and anchor each tooth into the alveolar process (Latin: para = adjacent to; Greek: odus = tooth).
The periodontium consists of the investing and supporting tissues of the tooth (gingiva, periodontal ligament, cementum, alveolar bone). The cementum is considered to be part of the periodontium because, along with the bone, it serves as the support for the fibers of the periodontal ligament. The periodontium is subject to morphologic and functional variations, as well as changes associated with aging.
Periodontal Diseases
Gingivitis — Periodontitis
There are numerous diseases that affect the periodontium. By far thé most important of these are plaque-associated gingivitis (gingival inflammation without attachment loss) and periodontitis (inflammation-associated loss of periodontal supporting tissues).
Gingivitis is limited to the marginal, supracrestal soft tissues. It is manifested clinically by bleeding upon probing of the gingival sulcus, and in more severe cases by erythema and swelling, especially of the interdental papillae.
Gingivitis is characterized by plaque-induced inflammation of the papillary and marginal gingivae. Clinical symptoms include bleeding on probing, erythema, and eventual swelling. Gingivitis may be more or less expressed depending on the
plaque - a biofilm — (quantity/quality) and the host response. Deeper-lying structures (alveolar bone, periodontal ligament) are not involved. Gingivitis may be a precursor to periodontitis, but this does not always occur.
Periodontitis can develop from a pre-existing gingivitis in patients with compromised immune status, the presence of risk factors and pro-inflammatory mediators, as well as presence of a predominately periodontopathic microbial flora. The inflammation of the gingiva may then extend into the deeper structures of the tooth-supporting apparatus. The consequences include destruction of collagen and loss of alveolar bone (attachment loss). The junctional epithelium degenerates into a “pocket” epithelium, which proliferates apically and laterally. A true periodontal pocket is formed. Such a pocket is a predilection site and a reservoir for opportunistic, pathogenic bacteria; these bacteria sustain periodontitis and enhance the progression of the disease processes.
Periodontitis is usually a very slowly progressing disease (Locker & Leake 1993; Albandar et al. 1997), which in severe cases — particularly when untreated — can lead to tooth loss. Enormous variation in the speed of progression of periodontitis is observed when one differentiates between individual patients. In addition to the quantity and composition of the bacterial plaque, individually varying influences also play important roles: patient’?, systemic health, patient’s genetic constitution, psychically influenced immune response status, ethnic and social factors, as well as risk factors such as smoking and stress ,r
In the aggressive forms of periodontitis, the manifestation of tissue loss on individual teeth occurs in successive acute phase? rather than, in a gradual, chronic, progression. Phases of progression and quiescence alternate. Destructive phases may occur rapidly one after another, or longer quiescent phases may be noticeable.
Gingival recession
Gingival recession is not actually a “disease,” but rather an anatomic alteration that is elicited by morphology, improper oral hygiene (aggressive scrubbing), and possibly functional overloading.
Teeth do not fall out due to classical gingival recession, but patients may experience cervical hypersensitivity and esthetic complications. If gingival recession extends to the mobile oral mucosa, adequate oral hygiene is often no longer pos? sible. Secondary inflammation is the consequence.
In addition to classical gingival recession, apical migration of the gingiva is often observed in patients with longstanding, untreated periodontitis, and it may be a consequence of periodontitis therapy in elderly patients (“involution”). These three periodontal disorders gingivitis, periodontitis, gingival recession — are observed world-wide; they affect almost the entire population of the globe to a greater
or lesser degree. In addition to these common forms of oral pathology, more rarely defects and diseases of periodontal tissues occur. All of these diseases were comprehensively classified at the international World Workshop in 1999.
Classification of diseases of the periodontium
Disease classifications are useful for the purposes of diagnosis, prognosis, and treatment planning. Different classifications of periodontal diseases have been used over the years and have been replaced as new knowledge improved our understanding of the etiology and pathology of the diseases of the periodontium.
Traditionally, periodontal diseases have been divided into two major categories: gingival diseases and periodontal diseases. The former includes diseases that attack only the gingiva, whereas the latter includes diseases that involve the supporting structures of the tooth.
Gingival diseases
Gingivitis (inflammation of the gingiva) is the most common form of gingival disease. Inflammation is almost always present in all forms of gingival diseases, because bacterial plaque, which causes inflammation, and irritating factors, which favor plaque accumulation, are often present in the gingival environment.
This has led to the tendency to designate all forms of gingival disease as gingivitis, as if inflammation were the only disease process involved.
The role of inflammation in gingival diseases varies in three ways:
Inflammation may be the primary and only pathologic change. This is, by far, the most prevalent type of gingival disease.
Inflammation may be a secondary feature, superimposed on systemically caused internal disease. For example, inflammation commonly complicates gingival hyperplasia caused by the systemic administration of phenytoin.
Inflammation may be the precipitating factor responsible for clinical changes in patients with systemic conditions that of themselves do not produce clinically detectable gingival disease. Gingivitis in pregnancy is an example.
Types of gingival disease
Gingival inflammation may be localized in all gingiva (generalized gingivitis) and may be located on a part of gingiva (localized gingivitis). In cases when inflammation affected one or two interdental papillae it’s called papillitis.
The most common type of gingival disease is the simple inflammatory involvement caused by bacterial plaque attached to the tooth surface. This type of gingivitis,
called chronic marginal gingivitis or simple gingivitis, may remain stationary for indefinite periods of time or may proceed to destroy the supporting structures (i.e., periodontitis). The reasons for these different behaviors are not clear.
These other types of gingival disease include the following:
1. Acute necrotizing ulcerative gingivitis, as well as gingival changes seen in acquired immunodeficiency syndrome (AIDS) patients.
2. Acute herpetic gingivostomatitis and other viral, bacterial, or fungal diseases.
3. Allergic gingivitis.
4. Skin diseases that also involve the gingival tissues, inducing characteristic types of gingival disease, such as in lichen planus, pemphigus, erythema multiforme, and other dermatoses.
5. Gingivitis that is initiated by bacterial plaque, but in which the tissue response is modified by systemic factors. Such is the case with nutritional deficiencies, endocrine diseases such as diabetes, and conditions such as pregnancy, puberty, and hematologic and immunologic problems,
6. Gingival enlargement, in which the gingival response to a variety of pathogenic agents results in an increase in volume. Drug-associated changes such as those induced by phenytoin, cyclosporine, and other drugs are included in this group.
7. Different benign and malignant tumors may appear in the gingiva either as primary tumors or as metastases.
Diseases of the tooth-supporting structures There are several different diseases that involve the tooth-supporting tissues. Many older classifications considered them in terms of the pathologic changes they produced (e.g., inflammatory, degenerative, or neoplastic). Although there are degenerative and neoplastic periodontal diseases, the-most common disease, by far, is initiated by plaque accumulation in the gingivodental area and is basically inflammatory in character. Initially it is confined to the gingiva and is called chronic marginal gingivitis. Later the supporting structures become involved, and now the disease is termed periodontitis. There is a continuum of changes from marginal gingivitis to periodontitis, and the term periodontal disease has been used genetically to refer to the entire process and more specifically to refer to periodontitis. The term chronic destructive periodontitis, however, is more accurate designation for this disease.
The periodontal tissues can also be involved by other nosologic entities unrelated to plaque; many of these fall into the degenerative or neoplastic categories. These diseases often involve other organs or systems and are considered periodontal manifestations of systemic diseases; these may have their initiation in the gingival tissues, in the underlying supporting structures, or both.
Periodontitis
Periodontitis is the most common type of periodontal disease and results from extension of the inflammatory process initiated in the gingiva to the supporting periodontal tissues. Synonyms, which are not currently in use, include Schmutz pyorrhea (Gottlieb), paradentitis (Weski, Beck), paradentosis, periodontoclasia, pericementitis, parodontitis, alveolar pyorrhea, alveoloclasia, Riggs’ disease, and chronic suppurative periodontitis.
Periodontitis has been classified according to the rate of progression (slowly progressive and rapidly progressive) and according to the age at onset (adult periodontitis and early-onset periodontitis). Other forms are necrotizing ulcerative periodontitis and refractory periodontitis.
Classification of chronic destructive periodontitis
1. Periodontitis
A. Slowly progressive periodontitis
B. Rapidly progressive periodontitis Adult onset periodontitis
Early onset periodontitis
a. Prepubertal periodontitis
b. Juvenile periodontitis
C. Necrotizing ulcerative periodontitis
D. Refractory periodontitis
II. Trauma from occlusion
III. Periodontal atrophy
IV. Periodontal manifestations of systemic diseases
In Ukraine there is periodontal diseases classification by N. Danylevsky (1994):
I. Inflammatory diseases
1. Gingivitis
This is mainly such forms as catarrhal, hypertrophic or ulcerous inflammation.
2. Localised periodontitis
This is such forms as catarrhal, hypertrophic or ulcerous inflammation.
II. Distrophic-inflammatory diseases
1. Generalized periodontitis,
I Chronic or exacerbative course Degree of development: I, II, III degree
2. Periodontosis
III. Progressive idiopathic diseases
IV. Productive periodontal diseases
Gingival inflammation (gingivitis)
Catarral gingivitis
It develops more often as a result of acute injury caused by fish bones, toothbrush bristle, dental instruments when treating teeth, etc. The most common local etiological factors are overhanging restorations edges and food impaction.
Acute catarrhal gingivitis. Patients often complain of pain, gum reddening and bleeding.
The act of discoloring at acute gingival inflammation differ in both nature and distribution from those at chronic gingivitis. The discoloration may be marginal, diffuse or patch-like, depending on the underlying exacerbation. Color changes according to the intensity of the inflammation. In all instances there is an initial bright red erythema.
On probing the hyperemia, edema, bleeding may be revealed. Some of the former stipping gingival papillae are lost.
Chronic catarrhal gingivitis. Thus, chronic inflammation intensifies red or bluish red; this is caused by vascular proliferation and reduction of keratinization owing to epithelial compression with the inflamed tissue. Venous stasis will add a bluish hue. Originally light red, the color changes to varying shades of red, reddish blue, and deep blue with increasing chronic inflammatory process. The changes start in the interdental papillae and gingival margin and spread to the attached gingiva.
Both chronic and acute inflammations produce changes in the normal firm and supple consistency of the gingiva. As noted, at chronic gingivitis both destructive (edematous) and reparative (fibrotic) changes coexist, and the consistency of the gingiva is determined by their relative predominance
Gingival enlargement (hypertrophic gingivitis)
Chronic inflammatory gingival enlargement is caused by prolonged exposure to dental plaque. Factors that favor plaque accumulation and retention include poor
oral hygiene, abnormal relationships of adjacent teeth and opposing teeth, lack of tooth function, cervical cavities, overhanging margins of dental restorations, improperly contoured dental restorations or pontics/ food impaction, irritation from clasps or saddle areas of removable prostheses, nasal obstruction, orthodontic therapy involving repositioning of teeth, and habits such as mouth breathing and pressing the tongue against the gingiva. In some cases inflammation initiated by dental plaque on background system diseases which include some hormonal conditions (e.g., pregnancy and puberty), i
Hypertrophic gingivitis has chronic course and is rarely exacerbated. The enlargement is limited to interdental papillae or marginal gingiva.
Patients usually do not complain of pain, rarely it arises from mechanical irritants. Overgrowing gingival papillae densely fill interdental spaces. The gingival papillae tissue is mulberry shaped, firm, pale pink, and resilient, with a minutely lobulated surface. On probing bleeding may be revealed.
The gingival papillae enlargement may be traumatized by teeth-antagonists and interfere with occlusion. Depending on gingival enlargement the following degrees are distinguished: I degree — enlargement within the limits of 1/3 heights of tooth crown; II degree — within the limits of 1/2 and III degree— covers more than 2/3 heights of tooth crown.
Clinical features. Chronic inflammatory gingival enlargement arises as a slight ballooning of the interdental papillae and/or marginal gingiva. At the early stages it forms a life preserver-like bulge around the involved teeth. This bulge increases in size until it covers a part of the crown. The enlargement is usually papillary or marginal and may be localized or generalized. It progresses slowly and painlessly unless it is complicated by acute infection or trauma.
Gingival fibromatosis is a rare condition of undetermined etiology. It has been designated by such terms as gingivomatosis, elephantiasis, diffuse fibroma, familial elephantiasis, idiopathic fibromatosis, hereditary gingival hyperplasia, hereditary gingival fibromatosis, and congenital familial fibromatosis.
Clinical features. The enlargement affects the attached gingiva as well as the gingival margin and interdental papillae, in contrast to phenytoin-induced hyperplasia, which is often limited to the gingival margin and interdental papillae. The facial and lingual surfaces of the mandible and maxilla are usually affected, but the involvement may be limited to one of the jaws. The enlarged gingiva is pink, firm, and almost leathery in consistency and has a characteristic minutely pebbled surface. In severe cases the teeth are almost completely covered, and the enlargement spreads in oral vestibule. The jaws seem to be distorted because of the bul- bous enlargement of the gingiva. Secondary inflammatory changes are common at the gingival margins.
Acute necrotizing ulcerative gingivitis (ANUG) is inflammatory destructive disease of the gingiva that has characteristic signs and symptoms.
Etiology (Bacterial Flora). Plaut and Vincent in 1894 and 1896, respectively, introduced the concept that necrotizing ulcerative gingivitis is caused by specific bacteria, namely, fusiform bacillus and spirochetal organism.
Local predisposing factors are: dental plaques, calculus, defects in dental restorations and prostheses, malocclusion, etc. A poor diet has been mentioned as a predisposing systemic factor in NUG and its sequelae in developing.
Clinical Features. Necrotizing ulcerative gingivitis most often occurs as an acute disease. Its relatively mild and more persistent form is referred to as subacute disease. Recurrent disease is marked by periods of remission and exacerbation. A reference is sometimes also made to chronic necrotizing ulcerative gingivitis.
Oral signs. Characteristic lesions are punched out, crater-like depressions at the crest of the interdental papillae, subsequently extending to the marginal gingiva and rarely to the attached gingiva and oral mucosa. The surface of the gingival craters is covered by a gray, pseudomembranous slough, demarcated from the remainder of the gingival mucosa by a pronounced linear erythema. In some cases, the lesions of the pseudomembrane surface are denuded, exposing the gingival margin, which is red, shiny, and hemorrhagic. The characteristic lesions may progressively destroy the gingiva and underlying periodontal tissues.
Spontaneous gingival hemorrhage or pronounced bleeding on the slightest stimulation are additional characteristic clinical signs. Other signs often found are: fetid odor and increased salivation.
Patients are usually ambulatory and have a minimum of systemic complications. Local lymphadenopathy and a slight elevation in temperature are common features of the mild and moderate stages of the disease. In severe cases there may be marked systemic complications such as high fever, increased pulse rate, leukocytosis, loss of appetite, and general lassitude. Systemic reactions are more severe in children. Insomnia, constipation, gastrointestinal disorders, headache, and mental depression sometimes accompany the condition.
In very rare cases, severe sequelae such as noma or gangrenous stomatitis have been described.
Gingivitis treatment
The treatment of acute gingival disease entails the alleviation of the acute symptoms and elimination of all other periodontal diseases, both chronic and acute, throughout the oral cavity. Treatment is not complete if periodontal pathologic changes or factors capable of causing them are still present. The most severe is necrotizing ulcerative gingivitis, therefore, its treatment is described below.
The treatment of NUG consists in: (1) alleviation of acute inflammation by reducing the microbial load and removal of necrotic tissue; (2) treatment of chronic disease either underlying the acute involvement or elsewhere in the oral cavity; (3) alleviation of generalized symptoms such as fever and malaise, and (4) correction of systemic conditions or factors that contribute to the initiation or progression of the gingival changes. ;
Sequence of Treatment
Treatment of NUG should follow an orderly sequence, according to specific steps in three clinical visits.
1. Mouthrinse with a glassful of an equal mixture of 3 % hydrogen peroxide and warm water, chlorhexidine digluconate solution.
2. Application of topical anesthetic: 2 % novocaine, lidocaine, prilocaine, ar- ticaine solution, etc.
3. Removing necrotic tissue with application protheolitic enzymes (trypsi- num, etc.).
4. Antibacterial therapy: erythromycin (500 mg every 6 hours) or metronidazole (500mg twice daily for 7 days).
5. Anti-inflammatory therapy: ibuprofen, indomethacin, naproxen, ketorol, natri imefenaminatis, etc.
6. Stimulation of regeneration: ascorbic acid (vitamin C), methyluracilum, etc.
7. Stimulation of epithelization: vitamin A and its preparations (oleumrosae, etc.).
Systemic antibiotics and topical antimicrobials
Antibiotics are administered systemically only in patients with systemic complications or local adenopathy. Antibiotics are not recommended for NUG patients who do not have these complications. A large variety of drugs have been used in the treatment of NUG. Topical drug therapy is only an adjunctive measure; no drug, when used alone, can be considered complete therapy. When used, systemic antibiotics also reduce the oral bacterial flora and alleviate the oral symptoms, but they are only an adjunct to the complete local treatment that the disease requires. Patients treated by systemic antibiotics alone should be cautioned that the acute painful symptoms may recur after the drug is discontinued.
Generalized periodontitis
Periodontitis can develop from a pre-existing gingivitis in patients with compromised immune status, the presence of risk factors and pro-inflammatory mediators, as well as the presence of a predominately periodontopathic microbial flora. The inflammation of the gingiva may then extend into the deeper structures of the tooth-supporting apparatus. The consequences include destruction of collagen and loss of alveolar bone (attachment loss). The junctional epithelium degenerates into a “pocket” epithelium, which proliferates apically and laterally. A true periodontal pocket is formed. Such a pocket is a predilection site and a reservoir for opportunistic, pathogenic bacteria; these bacteria sustain periodontitis and enhance the progression of the disease processes.
Periodontitis is usually a very slowly progressing disease, which in severe cases — particularly when untreated — can lead to tooth loss. Enormous variation in the speed of progression of periodontitis is observed when one differentiates between individual patients. In addition: to the quantity and composition of the bacterial plaque, individually varying influences also play important roles: patient’s systemic health, patient’s genetic constitution, psychically influenced immune response status, ethnic and social factors, as well as risk factors such as smoking and stress.
In the aggressive forms of periodontitis, the manifestation of tissue loss on individual teeth occurs in successive acute phases rather than in a gradual, chronic progression. Phases of progression and quiescence alternate. Destructive phases may occur rapidly one after another, or longer quiescent phases may be in noticeable.
Etiologic risk factors for gingival and periodontal diseases Oral Hygiene. The strong positive association that exists between poor oral hygiene and gingival and periodontal disease makes poor oral hygiene the primary etiologic agent. Statistically as well as clinically, bacterial plaque is a primary etiologic factor for periodontal disease. Therefore, poor oral hygiene is important risk factor in highly susceptible individuals and is of less importance in individuals with strong host resistance.
The incidence and severity of periodontal disorders are lower in individuals who receive regular dental care. The prevalence and severity of disease increase in patients which neglect dental care.
Small amounts of plaque that are not discernible on the tooth surface may be detected by running a periodontal probe or explorer along the gingival third
of the tooth. Another common method of detecting small amounts of plaque is the use of disclosing solutions
The strong association previously described between plaque and calculus and periodontal disease in its initial stages may be explained by the dynamics of plaque and gingivitis formation over time.
Microbiologic studies support the concept that chronic periodontitis is associated with specific bacterial agents. Microscopic examination of plaque from sites with periodontitis has consistently revealed elevated proportions of spirochetes. Cultivation of plaque microorganisms from sites of chronic periodontitis reveals high percentages of anaerobic (90 %) gram-negative (75 %) species.
The cause of gingival inflammation is bacterial plaque. Several factors previously considered to be of direct etiologic significance in periodontal disease are now known to act only by favoring plaque accumulation. These include calculus, faulty restorations, partial removable prostheses, and food impaction.
Although the acquired bacterial coatings have been demonstrated to be the major etiologic factor in periodontal disease, the presence of calculus isiof great concern for clinician. The primary effect of calculus is not, as may have been originally thought, of mechanical irritation but of bacteria that cover it. However, these calcified deposits play major role in maintaining and accentuating periodontal disease by keeping plaque in close contact with the gingival tissue and creating areas where plaque removal is impossible.
Defects in dental restorations and prostheses, referred to as iatrogenic factors, • are common causes of gingival inflammation and periodontal destruction. Inadequate dental procedures may also injure the periodontal tissues. Six characteristics of restorations and partial dentures are important from the periodontal viewpoint: margins of restorations, contours, occlusion, materials, design of removable partial dentures, and restorative procedures themselves.
Depending on its nature, malocclusion exerts a varied effect on the etiology of gingivitis and periodontal disease. Irregular alignment of teeth will make the plaque control difficult or even impossible. Uneven marginal ridges of contiguous posterior teeth have been found to have a low correlation with pocket depth, loss of attachment, plaque, calculus, and gingival inflammation.
Nutrition. The nutrients, that have been specifically associated with the periodontal tissues, are: vitamins A, B complex, C, and D, and calcium and phosphorus. Deficiencies in each of these nutrients and their effects on the periodontium have been clearly demonstrated in properly designed animal studies.
Protein deficiency also accentuates the destructive effects of local irritants and occlusal trauma on the periodontal tissues, but the initiation of gingival inflammation and its severity depend on the local irritants.
Hormonal disturbances may affect the periodontal tissues directly, as periodontal manifestations of endocrine diseases; modify the tissue response to plaque in gingival and periodontal diseases; or produce anatomic changes in oral cavity that may favor plaque accumulation or trauma from occlusion. Diabetes is an extremely important disease from the periodontal standpoint. A variety of periodontal changes have been described in diabetic patients, such as a tendency toward abscess formation, diabetic periodontoclasia, enlarged gingiva, sessile or pedunculated gingival polyps, polypoid gingival proliferations, and loose teeth.
In aged individuals, arteriosclerotic changes characterized by intimal thickening, narrowing of the lumen, thickening of the media, and hyalinization of the media and adventitia, with or without calcification, are common in vessels throughout the jaws, as well as in areas of periodontal inflammation. Both periodontal disease and arteriosclerosis increase with age, and it has been hypothesized that the circulatory impairment induced by vascular changes may increase the patient’s susceptibility to periodontal disease.
The clinical manifestations of periodontal diseases occur because of a complete interaction between the etiologic agents, in this case, specific bacteria found in dental plaque and the host tissues; There are many different factors which, locally or systemically, can influence the diseases course by modifying the process inherent in the bacterial-host interaction.
Clinical features of generalized periodontitis
Clinical features of generalized periodontitis can be presented in cardinal signs or complex of symptoms (I. Lucbmsky, 1945). They include:
• symptomatic gingivitis;
• periodontal pocket;
• trauma from occlusion (traumatic occlusion);
• progressive resorption of alveolar bone.
Symptomatic gingivitis develops on the background of other complex of symptoms. There are mainly such forms as catarrhal, hypertrophic or ulcerous inflammation. Catarrhal gingivitis develops in more than 70 % of patients with generalized periodontitis. Characteristic clinical features are: exudative inflammation of gingival mucosa, hyperaemia, epithelial cells desquamation, increasing vessels permeability, chronic or exacerbative course.
Another clinical feature of symptomatic gingivitis is hypertrophic gingivitis, mainly the granulating form. It is characterized by gingival enlargement, especially of interdental papillae, red or bluish red color, marked softness and friability, with ready fragmentation and bleeding when probing and pinpoint surface areas of redness and desquamation. The lesion is mulberry shaped, soft, red, and resilient, with a minutely lobulated.
Symptomatic ulcerative gingivitis usually has chronic course. Characteristic lesions are punched out, crater-like depressions at the crest of the interdental papillae, subsequently extending to the marginal gingiva and rarely to the attached gingiva and oral mucosa. The surface of the gingival craters is covered by a gray, pseudomembranous slough, demarcated from the remainder of the gingival mucosa by a pronounced linear erythema. In some cases, the lesions of the pseudomembrane surface are denuded, exposing the gingival margin, which is red, shiny, and hemorrhagic. The characteristic lesions may progressively destroy the gingiva and underlying periodontal tissues. Spontaneous gingival hemorrhage or pronounced bleeding on the slightest stimulation are additional characteristic clinical signs.
V-shaped symptomatic gingivitis develops in places with sustained severe mechanical irritation.
Periodontal pocket is one of the important clinical features of periodontal disease. Pockets can be classified as follows:'
Gingival Pocket (Relative or False) : This type of pocket is formed by gingival enlargement without destruction of the underlying periodontal tissues. The sulcus is deepened because of the increased bulk of the gingiva.
Periodontal Pocket (Absolute or True): This type of pocket occurs with destruction of the supporting periodontal tissues. Progressive pocket deepening leads to destruction of the supporting periodontal tissues and loosening and exfoliation of the teeth.
Trauma from occlusion. Trauma from occlusion may be a factor in determining the dimension and shape of bone deformities. It may be the second cause of periodontal destruction. Trauma from occlusion can result in bone destruction in the absence or presence of inflammation.
Trauma from occlusion is the occlusal interrelations of separate teeth groups or dental arches, which are characterized by supracontacts, interfering with closure in intercuspal position, uneven distribution of masticatory forces with pathologic teeth migration, pathological changes of periodontium, parafunctions of the masticatory musculature and temporomandibular joints.
Bone loss and bone destruction. The height of the alveolar bone is normally maintained by an equilibrium, regulated by local and systemic influences between b°ne formation and bone resorption. When resorption exceeds formation, bone height is reduced.
The level of bone is the consequence of past pathologic experiences, whereas changes in the soft tissue of the pocket walls reflect the present inflammatory condition. Therefore, the degree of bone loss is not necessarily correlated with the depth of periodontal pockets, the severity of ulceration of the pocket .wall, or the presence or absence of pus.
After the inflammation reaches the bone by extension from the gingiva, it spreads into the marrow spaces and destroys the alveolar bone.
Alveolar bone resorption develops slowly and depends on its level resulting in different clinical symptoms: gingival recession and pathologic tooth mobility. Pathologic tooth mobility is important clinical feature of periodontal disease. The degrees of pathologic tooth mobility by D. Entin can be distinguished as follows: grade I — tooth mobility in vestibular-lingual direction; grade II — in vestibular- lingual and medial-distal direction; grade III — in vestibular-lingual, medial-distal direction and vertical direction.
Alveolar bone resorption leads to different degrees of gingival recession.
It is possible to define the approximate depth of resorption, which clinically depends on the size of gingival recession, however the most exactly it would be revealed by means of radiographic examination. The level of resorption of interdental septa is a clinical sign of pathologic process in periodontium. A few degrees of interdental septa resorption are distinguished: initial, I, II and III degree. At the initial degree the resorption of alveolar bone is insignificant and is not accompanied by atrophy of in? terdental septa, at I degree the resorption occupies one-third of the interdental septa; at II degree the loss of bone tissue extends to the half of the height of interdental septa, and at III degree the loss occupies more than 2/3 of the interdental septa heights.
Clinical features
The characteristic sings at chronic periodontitis are: gingival inflammation, which results in accumulation of plaque, and loss of periodontal attachment and alveolar bone, which in turn results in formation of a pocket. In many patients the gingival inflammation is not visible during the inspection and can be detected only when probing.
The disease is usually generalized, although some areas may be involved more deeply than others. Areas of deeper involvement are usually associated with poorer plaque control and can be found in relatively inaccessible sites such as furcation areas or malposed teeth.
Gingival bleeding, either spontaneous or easily provoked, is frequent, and inflammation-related exudate and suppuration from the pocket may also be revealed.
When the pocket is sealed off, pus cannot drain, and an abscess may form. These localized areas of acute inflammation do not develop very often, but when they do, they need emergency care.
Pocket depths are variable, and both horizontal and angular bone loss can occur. Tooth mobility often occurs in neglected cases when bone loss is significant.
Symptoms. Chronic periodontitis is usually painless. Occasionally, exposed roots may be sensitive to the heat and/or cold in the absence of caries. Areas of localized dull pain, sometimes radiating deep into the jaw, are associated with chronic periodontitis. The presence of areas of food impaction may increase patient’ discomfort. Gingival tenderness or “itching” can also occur.
Acute pain may appear during the forming of periodontal abscess, and root caries or recurrent caries may result in pulpal symptoms.
Types. Mild periodontitis (I degree) is usually characterized by probing attachment loss of 2 to 4mm, minimal furcation invasions, and little tooth mobility. Along with various amounts of calculus supra— and subgingival plaque are present. Bleeding on gentle probing is frequently observed. Radiographic, evidence of bone loss is minimal (usually less than 20 % of the total attachment). This stage of involvement can be localized to several teeth or generalized to many areas throughout the mouth.
Patients with moderate periodontitis (II degree) exhibit 4 to 7 mm of probing attachment loss, early to moderate furcation invasions, and slight to moderate tooth mobility. Radiographically evident bone loss is usually horizontal and may consist of up to 40 % of the total periodontal attachment on the tooth.. Furcation radio- lucencies may be evident. Bleeding on probing and purulence may be frequently observed.
Patients with severe periodontitis (III degree) have a probing attachment loss of 7 mm or more with significant furcation invasions, often through-and-through hole of the furcation. Excessive tooth mobility is usually observed. Radiographically evident bone loss , exceeds 40 %, and angular bony defects are seen. Along with bleeding on probing purulent exudate can be present.
Radiographs in diagnosis of periodontal disease. The radiograph is a valuable aid in the diagnosis of periodontal disease, determination of the prognosis and evaluation of treatment outcome.
Radiographic changes in periodontitis.
1* Fuzziness and a break in the continuity of the lamina dura at the mesial or distal aspect of the crest of the interdental septum have been considered as the earliest radiographic changes in periodontitis. These result from the extension of gingival inflammation into the bone causing widening of the vessel channels and reduction in calcified tissue at the septal margin.
2. A wedge-shaped radiolucent area is formed at the mesial or distal aspect of the crest of the septal bone. The apex of the area is pointed in the direction of the root. This is produced by bone resorption of the lateral aspect of the interdental septum.
3. The destructive process extends across the crest of the interdental septum and the height is reduced. Fingerlike radiolucent projections extend from the crest into the septum. They are the result of the deeper extension of the inflammation to the bone.
4. The height of the interdental septum is progressively reduced by the extension of inflammation and the resorption of bone.
Treatment of periodontal diseases
General principles of treatment. Treatment of patients with periodontal diseases must be complex, purposeful and strictly individualized. It includs local and systemic treatment, effective conservative (medicamental), surgical, prosthetic, orthdontic and physical therapy methods and maintenance phase (recall). The complex treatment should generally be, primarily etiologic, pathogenetic and, finally, symptomatic.
The complex treatment of periodontal diseases may be divided into a few kinds or stages:
1. Initial medication treatment (antibiotic coverage).
Emergency treatment. Emergency procedures are performed in cases of acute necrotizing ulcerative gingivitis (ANUG), periodontal abscesses, periodontic-endodontic lesions (acute pulpitis, apical periodontitis), etc.
3. Patient motivation and training to the rational oral hygiene.
4. Complete elimination of all dental plaque, calculus, iatrogenic irritants and plaque-retentive areas; polishing root surfaces, old restorations, open furcations in multirooted teeth, etc.
Sequence of treatment. Following clinical examination and determination of prognosis a case presentation is made. The patient is informed about diagnosis, severity of disease, the necessity of treatment and phases of treatment. During the case presentation, dentists should begin to collect the subjective signs indicating the patient’s desire to cooperate.
Traumatic lesions of oral mucosa. ReasonsT Clinic. Diagnostics. First aid.
Mechanical injury
Acute mechanical injury (trauma mechanicum acutum) of mucosa membrane appears under the short-term strong influence -t-h by chance with the biting, the impact or the injury by different objects. Most frequently mucosa membrane of the tongue, lips and cheeks along the line of teeth joining suffer. In this case at first pain appears, and on the place of injury hematoma, excoriation, erosion or ulcer can be formed. Frequently their sizes, form and localization on mucosa membrane coincide with the same of the traumatic agent.
Complaints:
• Insignificant pain, burning, smarting of mucous membrane in the region fig oftheinjury;
• Painful section of the mucous membrane changes its colour in the place of the injury;
• Slightly painful cyanotic formation, which arises after sudden injury. Sharp pain, bleeding from the damaged section.
Stages of the treatment
1. Elimination of the local traumatic factor and its consequences.
2. Anesthetization.
3. Antiseptic processing.
4. Application of the epithelializing medicines.
Chronic mechanical injury (trauma mechanicum chronicum)
Complaints:
• sensation of discomfort, pain, swelling;\
• frequent biting;
• presence of the old ulcer;
• Growth in the hard palate, the gums, the tongue, under the prosthesis.
• Whitish section of the mucous membrane in the place of the permanent traumatic factor
Clinic:
• Lymph nodes are increased, painful during palpation. The manifestation of changes depends on gravity of the lesion.
• Inflammatory spot or erythema in the place of the injury.
• Localization of erosion corresponds to the traumatic agent, erosion is painful, localized on the hyperemized mucous membrane.
• Indolent ulcer is localized more frequently on the tongue, lips, cheeks along the line of teeth joining, and also in the limits of orthopaedic field. It is single, painful, surrounded with inflammatory infiltration, the bottom is most often uneven, covered with fibrinous fur. The decrease, the disappearance of painfulness, the appearance of papillary growths indicate about malig- nization.
• Papillomatous hyperplasia — papilloms with the soft, grainy, bright red surface under the prosthesis, they are more frequent localized in the region of the hard palate.
• With the habit to bite or to suck lips, tongue, and cheeks mucosa membrane (in essence along the line of teeth joining) acquires the unique form: it will swell, it has the white macerated surface in the form of either spots and large illegibly limited sections, or fringed form because of many small patches of the unevenly biting epithelium. Lesion has asymptomatic course, but during the deep removal the erosions are formed, they are painful in contact with chemical stimuli.
Treatment:
1. The elimination of the traumatic agent.
2. Anesthetization.
3. Cleaning the surface of erosion and ulcer from the necrotic fur.
4. Processing of ulcer and oral cavity by the solutions of the antiseptics.
5. Stimulation of the epithelisation.
Chemical injury
Chemical damage (trauma chymicum) appears when chemical substances enter oral mucosa. It can be acute and chronic. Acute chemical damage appears when chemical substances with sufficiently high concentration enter oral mucosa. Most often this happens when using them erroneously at home, in industry, when attempting suicide, during a visit to a dentist. The bums of oral mucosa can arise during the contact with acids, alkalis, the use of arsenic paste, phenol, formalin,
formalinresorcinol mixture, nitrate of silver. The clinical picture of lesion (hyperemia, edema, erosion, necrosis, and ulcer) depends on the nature of the chemical substance, its quantity, concentration and action time. With the bums of acids coagulation necrosis appears, with alkalis — colliquative necrosis (lesion is deeper and can affect all layers of soft tissues).
Clinic of the coagulation necrosis: Media damage:
• hyperemia, .
• edema,
• necrosis of tissues,! *
• forming of dense necrotic film,
• erosion,
• ulcer in the limits of the layers of mucous membrane, rarely the necrosis of the part of the alveolar branch (in contact with arsenous acid),
• dense brown film (layer) 4s formed in cbntact with sulfuric acid, yellow — nitric, grey-white — other acids.
Clinic of the colliquative necrosis:
• hyperemia, i tip. i lijHlii
• edema,
• necrosis of tissues,
• forming of loose necrotic masses,
• deep ulcer, which affects all layers of mucous membrane.
Treatment.
It is necessary to remove the damaging chemical substance at once and to wash the oral cavity with the dilute solution of the neutralizing agent. To treat acid burns soap water, 1 % lime water, burnt magnesia, 0.1 % solution of ammonium hydroxide (15 drops to the glass of water) are used Alkalis is neutralized with 0.5 % solution of acetous or citric acid, and also with 0.1 % solution of hydrochloric acid (10 drops to a glass of water) and thus will stop further penetration of chemical substance into the tissues.
Further treatment of patients with chemical bums of oral mucosa carries out as treatment of the acute unspecific inflammatory process: prescribing anaesthetizing medicines, dilute solutions of the antiseptic medicines in the form of oral bathes, §arglings, the accelerating epithelization medicines (1 % solution of citral or peach °d, metiluratsil ointment, vitamins A and E).
Infectious diseases of oral mucosa: ulcerous stomatitis, candidiasis of oral mucosa, viral lesions
Acute necrotizing ulcerative gingivitis
Acute necrotizing ulcerative gingivitis (ANUG) is an endogenous oral infection that is characterized by necrosis of the gingiva. Occasionally, ulcers of the oral mucosa also occur in patients with hematologic disease or severe nutritional deficiencies.
Studies have shown that the disease is accompanied by an overgrowth of organisms prevalent in normal oral flora and is not transmissible. The organisms most frequently mentioned as working symbiotically to cause the lesions are the fusiform bacillus and spirochetes. Plaque samples taken from ANUG patients demonstrate a constant anaerobic flora of Treponema spp, Selenomonas spp, Fusobacterium spp, and Bacteroides intermedius. The tissue, destruction is thought to be caused by endotoxins that act either directly on the tissues or indirectly by triggering immunologic and inflammatory reactions.
Classic ANUG in patients without an underlying medical disorder is found most often in those between the ages of 16 and 30 years, and it is associated with three major factors:
1. Poor oral hygiene with pre-existing marginal gingivitis or faulty dental restorations.
2. Smoking.
3. Emotional stress.
Systemic disorders associated with ANUG are diseases affecting neutrophils (such as leukemia or aplastic anemia), marked malnutrition, and HIV infection. Malnutrition-associated cases are reported from emergent countries where the untreated disease may progress to noma, a large necrotic ulcer extending from the oral mucosa through the facial soft tissues.
A fulminating form of ulcerative stomatitis related to ANUG is noma (cancrum oris), which predominantly affects children in sub-Saharan Africa. This disease is characterized by extensive necrosis that begins on the gingiva and then progresses from the mouth through the cheek to the facial skin, causing extensive disfigurement. The major risk factors associated with noma include malnutrition, poor oral hygiene, and concomitant infectious diseases such as measles. Living in close proximity to livestock is also believed to play a role, and Fusobacterium necrophorum, a pathogen associated with disease in livestock, has been isolated from over 85 % of noma lesions. The mortality rate without appropriate therapy exceeds 70 %.
Clinical manifestations. The onset of acute forms of ANUG is usually sudden, with pain, tenderness, profuse salivation, a peculiar metallic taste, and spontaneous bleeding from the gingival tissues. The patient commonly experiences a loss of the sense of taste and a diminished pleasure from smoking. The teeth are frequently thought to be slightly extruded, sensitive to pressure, or to have a “woody sensation.” At times they are slightly movable. The signs noted most frequently are gingival bleeding and blunting of the interdental papillae. The typical lesions of ANUG consist of necrotic punchedout ulcerations, developing most commonly on the interdental papillae and the marginal gingivae. These ulcerations can be observed most easily on the interdental papillae, but ulceration may develop on the cheeks, the lips, and the tongue, where these tissues come in contact with the gingival lesions or following trauma. Ulcerations also may be found on the palate and in the pharyngeal area. When the lesions have spread beyond the gingivae, blood dyscrasias and immunodeficiency should be ruled out by ordering appropriate laboratory tests, depending upon associated signs and symptoms.
The ulcerative lesions may progress to involve the alveolar process, with sequestration of the teeth and bone. When gingival hemorrhage is a prominent symptom, the teeth may become superficially stained a brown color, and the mouth odor is extremely offensive. The tonsils should always be examined since these organs may be affected. The regional lymph nodes usually are slightly enlarged, but occasionally the lymphadenopathy may be marked, particularly in children.
The constitutional symptoms in primary ANUG are usually of minor significance when compared with the severity of the oral lesions. Significant temperature elevation is unusual, even in severe cases, and, when it exists, other accompanying or underlying diseases should be ruled out, particularly blood dyscrasias and AIDS. HIV-infected patients with NUG have rapidly progressing necrosis and ulceration first involving the gingiva alone, and then NUP with the periodontal attachment and involved alveolar bone. The ulcerated areas may be localized or generalized and often are very painful. In severe cases, the underlying bone is denuded and may become sequestrated, and the necrosis may spread from the gingiva to other oral tissues.
Treatment. The therapy of ANUG uncomplicated by other oral lesions or systemic disease is local débridement. At the initial visit, the gingivae should be dé- brided with both irrigation and periodontal curettage. The extent of the débridement depends on the soreness of the gingivae. The clinician should remember that the more quickly the local factors are removed, the faster is the resolution of the lesions. Special care should be taken by the clinician to débride the area just below the marginal gin— givae. Complete débridement may not be possible on the first visit because of soreness. The patient must return, even though the pain and other symptoms have disappeared, to remove all remaining local factors.
Treatment of ANUG is not finished until there has been a complete gingival curettage and root planing, including removal of overhanging margins and other predisposing local factors. After the first visits careful home care instruction must be given to the patient regarding vigorous rinsing and gentle brushing with a soft brush. Patients should be made aware of the significance of such factors as poor oral hygiene, smoking, and stress. r
Antibiotics are usually not necessary for routine cases of ANUG confined to the marginal and interdental gingivae. These cases can be successfully treated with local debridement, irrigation, curettage, and home care instruction including hydrogen peroxide (approximately 1.5 to 2 % in water) mouth rinses three times a day and chlorhexidine 12 % rinses. Antibiotics should be prescribed for patients with extensive gingival involvement, lymphadenopathy, or other systemic signs, and in cases in which mucosa other than the gingivae is involved. Metronidazole and penicillin are the drugs of choice in patients with no history of sensitivity to these drugs. Patients whose lesions have extended from the gingivae to the buccal mucosa, tongue, palate, or pharynx should be placed on antibiotics and should have appropriate studies to rule out blood dyscrasias or AIDS. After the disease is resolved, the patient should return for a complete periodontal evaluation. Periodontal treatment should be instituted as necessary . The patient must be made aware that, unless the local etiologic factors of the disease are removed, ANUG may return or become chronic and lead to periodontal disease.
Mycotic lesions
Candidiasis or candidomikosis of oral mucosa is the disease, caused by fungi — the saprophytes of the oral cavity (Candida albicans, C. pseudotropicalis, C. tropicalis, C. cruséi, C. quilliermondi)^ w\i\c\i with weakening the resistance of organism and barrier function of oral mucosa,'with the development of dysbacteriosis become pathogenic.
The state of the decreased immunological reactivity can be caused by:
• action of antibiotics, corticosteroids and cytostatic means,
• irradiation,
• development of tumors,
• blood diseases,
• pathology of gastrointestinal tract,
• disturbance of exchange of substances (diabetes, hypovitaminoses),
. AIDS, etc.
Acute pseudomembranous candidiasis
Acute pseudomembranous candidiasis of oral mucosa (oral moniliasis; candi- dosis acuta, soor) develops in children’s infancy, weakened by infectious diseases, by bronchitis, dyspepsias, and also in premature children. It develops in older weakened by rachitis, exudative diathesis, hypovitaminoses, etc. Causative agent of oral moniliasis is Candida Albicans. Besides autoinfection, the infection can be transmitted through the mother’s nipples, contaminated dummy and baby food.
Clinic. In children’s infancy mother focuses attention on appearance of white spots or white coagulated fur, which in essence is accumulated in the retentional zones in the form of platelets or film (layer) on mucosa membrane of the cheeks, lips, the tongue, and the palate. If oral moniliasis is caused by Candidapseudotropi- calis, fur has a foam nature.
With the mild course of oral moniliasis platelets are freely removed, leaving at its place the focus of hyperemia; with the severe the centres of the stratification of fur merge into the continuous filmy surfaces, which in the course of time thicken and spread into all sections of oral mucosa. This fur is not easily scaled with scantiness, and erythema, and sometimes 44t with bleeding erosions, revealed under it.
Acute atrophic candidiasis
Acute atrophic candidiasis (candidosis acuta atrophica) develops with the increased sensitivity of oral mucosa to the fungi of the class of Candida.
The clinical picture of acute atrophic candidiasis is characterized by xerostomia, fieiy-red colour and burning of oral mucosa, absence of fur. Sometimes an insignificant number of crusts is formed on the red border of lips. If acute candidiasis is not treated, chronic (hyperplastic or atrophic) candidiasis develops.
Chronic hyperplastic candidiasis
Chronic hyperplastic candidiasis (candidosis chronica hyperplastica) develops in people, which assume cytostatics, antibiotics, in patients with tuberculosis, pathology of the blood, AIDS. It is characterized by appearance of white platelets, merging into the continuous coagulated bedding, which in the course of time thicken and become yellowish.
Depending on the topography of lesion candidiasis glossitis, cheilitis, angular cheilitis (perleche), palatinite are distinguished. The most frequently this disease occurs on mucosa membrane of the angles of mouth, on the back of tongue, the soft
palate. Ehe course of chronic hyperplastic candidiasis is accompanied by dryness, hyperemia and edema of oral mucosa, the hypertrophy of the tongue papillae is possible in certain cases.
Chronic atrophic candidiasis
Chronic atrophic candidiasis (candidosis chronica atrophica) occurs more frequently in people, who use detachable plate prostheses and is characterized by reddening, edema, dryness and burning of mucosa membrane with the secretion of viscous saliva. The sufficiently frequent form of chronic atrophic candidiasis is candidiasis cheilitis (cheilitis candidosa) — the lesion of the entire surface of lips or its angular parts (candidiasis perleche).
Candidiasis cheilitis is characterized by edema, hyperemia, thinning, dryness of red border, with certain deepening of the transversely located grooves, with formation and rejection of fish-scales of different value from the surface of the lips.
Candidiasis perleche is characterized by maceration of skin in the area of angles of mouth, the presence of cracks, covered with a white coating, and also the burning and the pain when opening the mouth.
The treatment of candidiasis of oral mucosa is intended to eliminate the clinical signs of disease, remove the prerequisites of the development of fungi and appearance of candidiasis and increase of the resistibility of organism.
Viral lesions
Herpetic infection — one of the most common and not controlled viral infections of man is caused by the virus of herpes simplex;
The development of herpetic vesicle has 4 stages:
1. appearance of the hyperemized section on the skin and mucous membranes accompanied by more or less expressed sensation of burning, itch of numbness or tingling;
2. formation of vesicles in several hours after the appearance of hyperemia. Vesicles have semi-circling form and are filled with transparent contents, which then grow turbid, vesicular stage lasts from 4 to 7 days and is frequently accompanied by more or less expressed adenopathy;
3. formation of crusts from the scaled epidermis after vesicle collapse and its release from the contents. The zone of vesicle is hyperemized, sometimes edemat- ic. On oral mucosa the erosions remain, which can for a second time be infected;
4. recovery. Crusts are separated and droped off. At the places of precipitations, which rapidly passed, the reddening remains.
Chronic recurrent herpes
After the transferred primary herpetic infection the virus remains in the human organism, obviously, during the entire life. Disease passes into the latent phase of prolonged virus carrying, which is frequently accompanied by relapses — a recurrent form. In oral cavity — this is chronic recurrent herpetic stomatitis, gingivostomatitis, recurrent herpes of lips and herpetic recurrent ganglionevritis.
Chronic recurrent herpes occur predominantly in adult and each tenth child (12.5 %), who had primary herpetic infection.
Fairly often, regardless of the season, and no matter how much time passed since the previous precipitation, relapse occurs after injuries (injection, the imposition of matrix, biting, separation and dental treatment for orthopedic purposes), supercooling, acute respiratory disease, acute respiratory viral, disease, or a clear connection with the menstrual cycle, and the exacerbation of the chronic diseases of gastrointestinal tract is established.
Recurrent herpes of oral mucosa is more frequently localized on the hard palate, cheeks, the tongue. Precipitations are limited, with the typical dynamics of the process: vesicles appear in clusters, merge, burst? forming erosion with the poly- cyclic outlines. In the first twenty-four hours of existence the erosions are very painful and accompanied by the painful reaction of lymph nodes. The general state of patients, as a rule, is not disrupted.
Depending on the frequency of relapses the forms of recurrent herpes are distinguished:
• mild (1-2 relapses for a period of 3 years);
• moderate (1-2 relapses in 1 year),
• severe (4-5 relapses in a year or permanently).
A cytological examination reveals the neutrophilic leukocytes of different degree of dystrophia, and also the layers of epithelial cells with the phenomena of polymorphism and cell-monsters (gigantic polynuclear cells of herpes, the so- called cells of the ballooning degeneration).
Varicella-zoster virus infection Varicella zoster virus (VZV) is a herpes virus, and, like other herpes viruses, it causes both primary and recurrent infection and remains latent in neurons present ln sensory ganglia. VZV is responsible for two major clinical infections of humans: ohickenpox (varicella) and shingles (herpes zoster [HZ]).
Chickenpox is a generalized primary infection that occurs the first time an individual contacts the virus. This is analogous to the acute herpetic gingivostomatitis of herpes simplex virus. After the primary disease is healed, VZV becomes latent in the dorsal root ganglia of spinal nerves or extramedullary ganglia of cranial nerves. A child without prior contact with VZV can develop chickenpox after contact with an individual with HZ. In 3 to 5 of every 1,000 individuals, VZV becomes reactivated, causing lesions of localized herpes zoster. The incidence of HZ increases with age or immunosuppression.
Patients who are immunocompromised due to HTV disease, cancer chemotherapy, immunosuppressive drug therapy, or hematologic malignancy have an increased susceptibility to severe and potentially fatal HZ. These HZ infections may be deep-seated and disseminated, causing pneumonia, meningoencephalitis, and hepatitis; however, otherwise normal patients who develop HZ do not have a significant incidence of underlying malignancy. |
Clinical manifestations
General Findings. Chickenpox is a childhood disease characterized by mild systemic symptoms and a generalized intensely pruritic3 eruption of maculopapular lesions that rapidly develop into vesicles on-an erythematous base. Oral vesicles that rapidly change to ulcers may be seen, but the oral lesions are not an important symptomatic, diagnostic, or management problem. HZ commonly has a prodromal period of 2 to 4 days, when shooting pain, paresthesia, burning, and tenderness appear along the course of the affected nerve. Unilateral vesicles on an erythematous base then appear in clusters, chiefly along the course of the nerve, giving the characteristic clinical picture of single dermatome involvement. Some lesions spread by viremia occur outside the dermatome. The vesicles turn to scabs in 1 week, and healing takes place in 2 to 3 weeks. The nerves most commonly affected with HZ are C3, T5, LI, L2, and the first division of the trigeminal nerve. % \
When the full clinical picture of HZ is present with pain and unilateral vesicles, the diagnosis is not difficult. Diagnostic problems arise during the prodromal period, when pain is present without lesions. Unnecessary surgery has been performed because of the diagnosis of acute appendicitis, cholecystitis, or dental pulpitis. A more difficult diagnostic problem is pain caused by VZ virus without lesions developing along the course of the nerve (zoster sine herpete; zoster sine eruptione). Diagnosis in these cases is based on clinical symptoms and serologic evidence of a rising antibody titer.
HZ may also occasionally affect motor nerves. HZ of the sacral region may cause paralysis of the bladder. The extremities and diaphragm have also been paralyzed during episodes of HZ. The most common complication of HZ is postherpetic neuralgia, which is defined as pain remaining for over a month after the mucocutaneous lesions have healed, although some clinicians do not use the term postherpetic neuralgia unless the pain has lasted for at least 3 months after the healing of the lesions. The overall incidence of postherpetic neuralgia is 12 to 14 %, but the risk increases significantly after the age of 60 years, most likely due to the decline in cell-mediated immunity.
Oralfindings. Herpes zoster involves one of the divisions of the trigeminal nerve in 18 to 20 % of cases, but the ophthalmic branch is affected several times more frequently than are the second or third divisions. HZ of the first division Can lead to blindness secondary to comeal scarring and should be managed by an ophthalmologist. Facial and intraoral lesions are characteristic of HZ involving the second and third divisions of the trigeminal nerve. Each individual oral lesion of HZ resembles lesions seen in herpes simplex infections. The diagnosis is based on a history of pain and the unilateral nature and segmental distribution of the lesions. When the clinical appearance is typical and vesicles are present, oral HZ can be distinguished clinically from other acute multiple lesions of the mouth, which are bilateral and are not preceded or accompanied by pain along the course of one trigeminal nerve branch.
HZ has been associated; with dental anomalies and severe scarring of the facial skin when trigeminal HZ occurs during tooth formation. Pulpal necrosis and internal root resorption have also been related to HZ. In immunocompromised patients, large chronic HZ lesions have been described that have led to necrosis of underlying bone and exfoliation of teeth. HZ of the geniculate ganglion, Ramsay Hunt syndrome, is a rare form of the disease characterized by Bell’s palsy, unilateral vesicles of the external ear, and vesicles of the oral mucosa. Because oral lesions occurring without facial lesions are rare, isolated oral HZ can be misdiagnosed, particularly when erythema, edema, and nonspecific ulceration are seen without the presence of intact vesicles. In these cases* a cytology smear or viral culture is often necessary for diagnosis. An incorrect diagnosis can be made when prodromal pain is present prior to the appearance of the characteristic lesions. During this period, endodontic therapy, extractions, or other surgery may be performed unnecessarily. Similar problems occur in zoster sine eruptione.
Treatment Management should be directed toward shortening the course of the disease, preventing postherpetic neuralgia in patients over 50 years of age, and preventing dissemination in immunocompromised patients. Acyclovir or the newer antiherpes drugs valacyclovir or famciclovir accelerate healing and reduce acute pain, but they do not reduce the incidence of postherpetic neuralgia.35 The newer drugs have greater bioavailability and are more effective in the treatment of HZ. The use of systemic corticosteroids to prevent postherpetic neuralgia in patients over 50 years of age is controversial; a recent review of the data indicated a reduction of pain and disability during the first 2 weeks but no effect on the incidence or severity of post-herpetic neuralgia. Some clinicians advocate the use of a combination of intralesional steroids and local anesthetics to decrease healing time and prevent postherpetic neuralgia, but a controlled study of this therapy has not been performed. Effective therapy for postherpetic neuralgia includes application of capsaicin, a substance extracted from hot chili peppers.
Topical capsaicin is safe but must be used for a prolonged period to be effective and may cause a burning sensation of the skin. When topical capsaicin therapy is ineffective, use of a tricyclic antidepressant or gabapentin is indicated. Chemical or surgical neurolysis may be necessary in refractory cases.
AIDS
AIDS syndromum immunodefectionis aguisitae — the syndrome of the acquired immunodeficiency is contagious immunological disease of virus etiology:
Etiology. AIDS is caused by virus from the family of the retroviruses of the subfamily of lentiviruses named by taxonomical committee of WHO ( World Health Organization) HIV (Human immunodeficiency virus).
The mechanism of AIDS consists in the destruction by the virus of the immune system as a result of the infection and the loss of the T-helpers (T4), on cytoplasmic membrane of which there is the protein CD-4, which serves as receptor for HIV. With the introduction into the cell the virus changes it irreversibly, using genetic material of a cell for its own reproduction: formed DNA is included in the chromosomes of cells and is converted into provirus, which can exist in the inactive form or appear itself, synthesizing virus proteins. Becoming more active (during the total weakening of immunity), HIV begins to multiply rapidly, seizing T-helpers and causing their loss. As a result disruptions of equilibrium in the system T-helpers — T-supressors the latter begin to suppress immunity. Besides quantitative changes, in the system of T-lymphocytes the qualitative changes begin. The mechanism of the suppression of cellular immunity includes cytopathic action HIV, toxic action of its components, and also cytotoxic action of macroorganism on its own CD-4 the fraction of the T-lymphocytes, which acquired antigenic properties. On this background the opportunistic infections, whose development composes the clinical picture of AIDS, attack the defenceless organism.
Clinic. The existence of phases of course is characteristic for AIDS. The duration of incubative period varies from several (6-8) months to several years. Approximately for 50 % of patients it is 4 years.
CDC-centre (Georgia, the USA) and WHO (1988) proposed the following classification of the clinical stages of AIDS:
1. Incubation.
2. Acute HIV-infection.
3. Virus carrying: a) the persisting infection; b) generalized infection.
4. Lymphadenopathy.
5. AIDS-associated complex.
6. AIDS with the development of infection and tumors. ,
The classification of V. I. Pokrovskj (1989) distinguishes 4 stages in the course of the HIV-infection:
1. Incubation.
2. Stage of the primary manifestations:1 a) the phase of acute fever; b) asymptomatic phase; c) persisting generalized lymphadenopathy.
3. Stage of secondary diseases.
A. The loss of body mass is less than 10 %, the superficial fungus, bacterial or viral lesions of the skin and the mucous membranes, herpes Zoster, recurrent pharyngitis, sinusitises.
B. Progressive loss body mass is more than 10 %, unexplained genesis diarrhea, fever for more than 1 months, hairy leukoplakia, pulmonary tuberculosis, repeated or steadfast bacterial, fungal, viral and protozoal lesions of the skin and the mucous membranes, repeated or disseminated herpes zoster, localized Kaposi’s sarcoma.
C. The generalized bacterial, viral, protozoal parasitic diseases, pneumo- cystic pneumonia, candidiasis of the gullet, atypical micobacteriosis, extrapulmonary tuberculosis, cachexia, the disseminated Kaposi’s sarcoma, CNS lesions of different etiology.
4. Terminal stage.
Reflill and Bourke (1988), as objective basis for spread of symptoms and stages of disease, development of its gravity, propose to use a number of T4 lymphocytes in 1 mm3 of the blood and the stages are the following:
1. Incubation;
2. Asymptomatic;
3. Chronic lymphadenopathy for a period of 3-5 years — pre-AIDS;
4. The subclinical disturbances of the immunity (in 1 mm3 of the blood — contained 400 T4-lymphocytes);
5. The appearance of allergic reactions to the skin tests (the number of T4- lymphocytes in 1 mm3 of the blood is less than 300);
6. Immunodeficiency followed by lesion of the skin and mucous membranes — absence of hypersensitivity of the delayed action (the number of T4-lymphocytes < 200);
7. The generalized manifestations of immunodeficiency — HIV-indicator opportunistic infections and malignant tumors are developed (T4-lympho- cytes < 100).
The clinical picture of AIDS, first of all, is caused by the T-cell immune deficiency. Reduction in the activity of immune system leads to the activation of saprophytic microflora.
The first manifestation of AIDS after being infected is a lesion of oral mucosa.
Rapidly progressive parodontitis, acute ulceronecrotic gingivostomatitis? angular cheilitis are observed. Centres in the periodontium tend to cause osteomyelitis. Fairly often a violent reaction to the endodontic interferences is developed. The appearance of these signs can indicate a problem for the persons of the risk group long before manifestations of candidiasis and hairy leukoplakia.
Depending on the frequency of distribution the diseases of oral mucosa are distinguished as follows: candidiasis (88 %), herpetic lesions (11-^17 %), xerostomia (19—28 %), exfoliative cheilitis (9 %), ulcers (7 %), desquamative glossitis (6 %), hairy leukoplakia (5 %), the Kaposi’s sarkoma (from 4 to 50 %), hemorrhage.
Candidiasis of oral mucosa in case of AIDS has several forms: pseudo-membranous, at which a significant number of soft white centres are observed, which resemble flakes of the curdled milk and which can be easily removed by means of scarifying; hyperplastic — it resembles leukoplakia, accompanied by dense white lesions, soldered with the surface of the oral mucosa, and atrophic (erythematous). With this form the erythematous spots without the fur appear, on the background of which in some places the spots of hyperkeratosis can be revealed.
Among the bacterial infections fusospirochetosis takes place, which causes acute ulceronecrotic gingivitis in the frontal section. It occurs in patients with AIDS, carriers of antibodies, and seropositive persons. In the latter, furthermore^ in the periapical tissues the exacerbations of the centres of secondary infection appear, and in the parodontium destructive changes are possible, up to the sequestration of the alveolar bone.
Secondary virus agents cause hairy leukoplakia. This group includes herpes viruses, welding dribbles and condylomas. Hairy leukoplakia resembles the mild form of leukoplakia and whitish hair growths, which cannot be removed by scaling. They are mainly located along the edge of the tongue and sometimes they resemble chronic hyperplastic candidiasis. Ulcers and aphthae in the oral cavity in case of AIDS are more frequently localized on the palate and are caused by Cryptococcus neoformans (yeast, that gemmate and does not form mycelium). Single mucous capsules sometimes are observed.
In homosexuals the early (first) manifestation of AIDS in the oral cavity are: painful ulcers on mucous membrane of the palate and the tongue, connected with the cytomegalovirus infections (group of the herpes viruses), with a characteristic slow protracted course, recurrence, the absence of the effectiveness of treatment with using conventional procedures. Simultaneously the ulcerous-herpetic lesions of lips in Klein’s zone, and also on mucous membrane of the nose are observed. It is established that all early manifestations of AIDS in the oral cavity are steady and are difficult to treat.
Vascular tumor —f Kaposi’s sarcoma is the transmissible disease, which is characterized by multiple pigmented lesions. In patients with AIDS it is observed mainly in the oral cavity before the palate in 76 % of cases and is characterized by exophytic growth, painlessness, friable consistency (in the form of soft cyanotic nodule), high frequency of malignancy. Soft tissues have color from brown to bluish-red.
Berkitt’s lymphoma is localized on the lower jaw. Before its formation patients complain about the toothache, mucosal ulceration, growth of the submaxillary lymph nodes.
The resorption of the bone tissue at this time is roentgenologically observed.
In those, who abuse smoking, the, epidermoid carcinoma is observed, which is localized on the tongue or at the bottom of the oral cavity. With AIDS other new formations develop — lymphoreticular sarcoma, planocellular cancer, etc. Radiation and chemotherapy of the described new formations in case of AIDS are ineffective.
Diagnostics. Early diagnostics of AIDS is extremely important, since the latent period between infection and appearance of clinical signs of AIDS can be sufficiently prolonged.
Taking into account the complexity of laboratory diagnostics at the proposal of WHO (World Health Organization) in certain cases the diagnosis of AIDS can be based on clinical symptomatology. All clinical symptoms are proposed to divide into two groups — serious and insignificant (WHO, 1986).
In adults AIDS is diagnosed in the presence of minimum two serious symptoms coupled with at least one insignificant symptom in the absence of apparent reasons for immunosuppression, such as cancer, the severe form of the alimentary insufficiency of nourishment and other states of the established etiology.
1. Serious symptoms:
a) decrease in body weight to 10 % and more;
b) chronic diarrhea more than 1 month;
c) fever lasting more than 1 month (interrupting or constant).
2. Insignificant symptoms: H3
a) persistent cough lasting more than 1 month;
b) generalized multi-focal dermatitis
c) recurrent herpes Zoster;
d) candidiasis of the oral cavity and throat;
e) chronic progressive and disseminated herpes simplex; |
g) generalized lymphadenopathy.
When only Kaposi’s sarcoma or cryptococcal meningitis is present, the diagnosis of AIDS is established.
Indications for consideration of AIDS are:
1. Malignant new formations (Kaposi’s sarcoma, lymphoma).
2. Infections:
• Fungi: a) candidiasis, which involves oral mucosa, causing dysfunction of esophagus; b) cryptococcosis, which causes the diseases of lungs, CNS and the scattered infection.
• Bacterial infections (“atypical” micobacteriosis, caused by the forms, which differ from the agents of tuberculosis and leprosy).
• Viral infections: a) the cytomegalovirus, which causes the diseases of lungs, gastrointestinal tract, CNS; b) the herpes virus, which causes the chronic infection of mucous membranes ulcers, elevated temperature for a month and more; c) the progressive encephalopathy considered to be caused by papovavirus; d) viruses HTFV, which lead to the malignant regeneration ofT-cells.
• Simplest and the helminths: a) pneumonia, caused Pneumocystis carinii; b) the toxoplasmosis, which causes pneumonia or lesion of CNS; c) cryp- tosporidiosis, which causes intestinal diarrhea for more than one month; d) strongiloidosis.
There are 3 methods to prove the presence of virus in the organism: the cultivation of virus, identification of virus antibodies, and development of caption of antibodies to virus antigens (test ELISA — enzime linked immunosorbent assay).
Treatment. For dealing with AIDS new approaches are developed. They are based on the basic researches, connected with the concepts, which have appeared recently and are develop rapidly, and also on the new technologies (intracellular immunity» genetic therapy). These technologies concerning AIDS develop in three directions.
The first direction is based on the injecting of the gene, which synthesizes the product, which then is separated from the cells.
Another direction is connected with the synthesis of peptide. They do not exceed the limits of cells and competitorily block key processes in development of HIV. The third direction is based on injecting into the cells of the genes, which code antisenses and ribozyms, which respectively block or destroy RNA virus.
Among the medicines, which are registered in the arsenal of preparations for treating this contingent of patients, besides azidothymidine ([AZT]), are widely used suromin, NRA-23, atsiclovir, correctors of immunity (interleukin-2, gamma globulin, the stimulator of the function of T-lymphocytes, isoprinosine). To maintain the immune status the bone marrow transplantation is conducted.
The basic thing for the stomatologist during the treatment of such patients is rendering to symptomatic therapeutic aid and the sanitation of the oral cavity.
Forecast. The determination of the level of T-helper lymphocytes and relationship of T4/T8 have a very important significance for the forecast of AIDS. When the level of T4 is less than 200 in 1 mm3 of the blood, mortality exceeds 50 % in the first year after the manifestation of the clinical symptoms of AIDS. Spontaneous remission is not described. Disease persistently progresses and causes death.
Manifestations of specific infection (syphilis, tuberculosis) on oral mucosa
Syphilis
Syphilis is a classic disease with protean manifestations. There has been a significant rise in the prevalence of syphilis both in the developed and developing world during the past two decades, mainly as a disease associated with HIV infection and sexual promiscuity. The disease is caused by T. pallidum, the syphilis spirochete. There is a very high likelihood of human to human transmission of syphilis through unprotected sexual activity.
Syphilis has an incubation period of 10 to 90 days (average 3 weeks) and is characterized by four main clinical stages: primaiy, secondary, tertiary, and late or quaternary.
Primary Syphilis After the inital exposure to infection with T. pallidum, the spirochetes pass through the mucous membrane or skin and are then carried in the
blood throughout the body. After an incubation period of about 3 to 4 weeks, there develops, at the site of entry, an ulcerated lesion called a primary chancre: a flat, red, indurated, highly infectious ulcer with serous exudate. The typical lesion is painless, und edema of the surrounding tissues is usually present. The regional lymph nodes become enlarged about 2 weeks after the appearance of the chancre and on examination are firm, painless, and discrete, with a rubbery consistency. The chancre disappears spontaneously within 3 to 8 weeks.
Secondary Syphilis Approximately 2 months after healing, the secondary stage of syphilis usually develops, and in about one-third of patients, the primary chancre may be present at the same time. The signs of secondary syphilis are variable: generalized skin lesions in about 75 % of cases, mucosal ulcers in about 33 % of cases, generalized lymphadenopathy in about 50 % of cases, and systemic symptoms that are “influenza like”, including fever, headache, malaise, and general aches and pains. The skin lesions are found predominantly on the face, hands, feet, and genitalia and appear as dull red macular or papular spots.
Tertiary Syphilis Reactivation of syphilis can occur at any time 2 or 3 years after the date of first infection, but such late lesions of syphilis are rarely seen today. The characteristic lesion is the gumma, which is usually localized, single or multiple, varying in size from a pinhead to a lesion several centimeters in diameter. Gummas develop in the skin, the mucous membranes, and bones. These lesions are not infective as the tissue damage is due to a delayed type of hypersensitivity. The other organs involved in tertiary syphilis are the cardiovascular system and the nervous system.
Late or Quaternary Syphilis This condition is seen one to two decades after primary syphilis. The two main clinical forms of late syphilis are cardiovascular syphilis and neurosyphilis, with resultant pathology of the aorta and the nervous system, respectively.
Latent Syphilis This may be seen in some after many years without any symptoms. The disease lies dormant, without any clinical signs (except for positive serology), and may manifest as cardiovascular or neurosyphilis.
Congenital Syphilis T. pallidum is one of the few microorganisms that has the ability to cross the placental barrier; thus, the fetus may be infected during the second or third trimester from a syphilitic mother (either in the primary or secondary stage of syphilis). The disease will manifest in the infant as either (1) latent infection—no symptoms but positive serology; (2) early infection — lesions such as skin rashes, saddle nose, bone lesions, and meningitis appear up to the end of the second year of age; or (3) late infection— after the second year of age; lesions include Hutchinson’s incisors (notching of incisor teeth), mulberry molar teeth (due
to infection of the enamel organ in the fetus), interstitial keratitis, bone sclerosis, arthritis, and deafness.
Oral considerations
Primary Syphilis The normal site for the chancre is on the genitalia, but extragenital primary lesions occur in about 4 to 12 % of patients with syphilis. A chancre of the lip is the most common extragenital lesion, accounting for about 60 % of cases, and may present at the angles of the mouth. Most chancres in the male tend to be located in the upper lip and in the female on the lower lip. Other sites affected are the tongue and, to a lesser extent, the gingivae and tonsillar area. Intraoral chancres are usually slightly painful due to secondary bacterial infection, as are the enlarged lymph nodes in the submaxillary, submental, and cervical regions. The lesions are infectious, and transmission may occur by kissing, unusual sexual practices, and even intermediate contact with cups, glasses, and eating utensils. The differential diagnosis of primary syphilis includes ruptured vesicles of herpes simplex, traumatic ulcers, and carcinoma.
Secondary Syphilis Characteristic slightly raised, grayish white, glistening patches on the mucous membrane, so-called “mucous patches”, of the tongue, soft palate, tonsil, or cheek but rarely the gingival tissues are common in the secondary stage. Lesions on the larynx and pharynx may lead to hoarseness. The surface of these lesions is covered with a grayish membrane, which can be easily removed and contains many spirochetes. The ulcers may coalesce to give the characteristic “snail tracks” and mucous patches in about a third of those affected. These lesions, like the primary chancre, are highly infectious. Maculopapular eruptions have been described in the mouth and are confined mainly to the palate, but, occasionally, the entire oral mucosa may be involved. In recent years, the secondary syphilitic lesions found in the mouth have been noted as often atypical, due, in many cases, to inadequate treatment as a result of antibiotic therapy for an unrelated infection: Other manifestations are generalized lymphadenopathy and condylomata (warts) of the anus and vulva; rarely, periostitis, arthritis, and glomerulonephritis may be seen. The differential diagnosis of secondary syphilis includes aphthous ulcers, erythema multiforme, lichen planus, and tonsillitis. The secondary-stage lesions heal 2 to 6 weeks after the time they first appear.
Tertiary Syphilis The representative lesion of this stage is the “gumma”, which begins as a small, pale, raised area of the mucosa that ulcerates and rapidly progresses to a large zone of necrosis with denudation of bone and in the case of the palate may eventually perforate into the nasal cavity. The most common site for gumma formation is the hard palate, although the soft palate, lips, tongue, and face may be involved. The palatal lesions are usually midline, and in rare cases, the soft Palate may be involved. Gummas are painless and have no infectivity.
Occasional cases of syphilitic osteomyelitis involving the mandible and, less commonly, the maxilla have been described. This condition represents a gummatous involvement of bone with extensive necrosis. The condition is characterized by pain, swelling, suppuration and sequestration, and both clinically and radio- graphically, the condition may resemble pyogenic osteomyelitis. If the lesion ossifies, then the radiographic appearance of the affected area may be similar to that of an osteogenic sarcoma.
Atrophic or interstitial glossitis is another oral manifestation of tertiary syphilis. Clinically, there is atrophy of the filiform and fungiform papillae, which results in a smooth, sometimes wrinkled lingual surface. This appearance is probably due to obliterative endarteritis of the lingual vasculature, leading to circulatory deficiency. Loss of the protective papillae subjects the dorsum of the tongue to many noxious stimuli, and leukoplakia frequently develops. The relationship between syphilitic glossitis and carcinoma of the tongue is not clear.
Syphilis very rarely affects the salivary glands, but both secondary and tertiary lesions have been described in the parotid glands. The other main salivary glands have also been involved either on their own or together with the parotid. Patients with general paresis of the insane may have perioral tremors and fine irregular tremors of the tongue and fingers. Although an association between oral squamous cell carcinoma and syphilis has been suggested in early studies, this relationship remains unproven.
Congenital Syphilis The dental lesions of congenital syphilis are a result of infection of the developing tooth germ by T. pallidum. Since the deciduous teeth are usually well developed by the time the spirochetes invade the developing dental tissues, these teeth are minimally affected. The permanent teeth are at an early stage of development, and infection may result in the complete failure of development of a tooth or the production of malformed teeth. Early oral manifestations include diffuse maculopapular rash, periostitis (frontal bossing of Parrot), and rhinitis, whereas late features, manifesting at least 24 months after birth, comprise the hutchinsonian triad of interstitial keratitis of the cornea, sensorineural hearing loss, and dental anomalies. The most common dental manifestation of congenital syphilis is the so- called “mulberry molar” teeth, which are highly suggestive of prenatal syphilis. The first permanent molar teeth are usually involved and have roughened, dirty, yellow, hypoplastic, occlusal surfaces with poorly developed cusps and are smaller in size than normal. Hutchinson’s incisors are another manifestation of congenital syphilis. The upper central incisors are usually involved and have crescentic notches in the middle of their incisal edge. The tooth tends to be wider gingivally than at the incisal edge, giving a “screwdriver” appearance. The lower incisors show similar defects, but they are affected much less often than their maxillary counterparts. Of note, the maxillary incisors are more commonly affected than the mandibular ones. Infection of the developing bones of the face may lead to permanent facial deformities, which produce an open bite and a “dished” appearance to the face. Skin around the lips may show yellow discoloration soon after birth, leading to crack formation and eventual (Parrot’s) radial scars — rhagades — of the lips. Other, less common orofacial features include atrophic glossitis and a high, narrow palatal vault.
Diagnosis and Management Exudate from primary or secondary lesions may be collected in fine capillary tubes and examined using dark-ground microscopy for typically motile T. pallidum. This technique has limited value in lesions affecting the mouth since the oral commensal Treponema microdentium closely resembles T. pallidum. However, specific immunofluorescence tests, if available, are helpful in diagnosis.
The laboratory diagnosis of syphilis is usually made by serology since T. pallidum cannot be routinely cultured in vitro. Ten milliliters of venous blood is sufficient to carry out all the serologic tests for syphilis. It is usual to carry out at least two different tests on each specimen of serum, and the interpretation of these complex test results should be left to an expert in genitourinary infections. Antigens used for syphilis serology are of two types: treponemal antibody-absorption test (FTA-Abs), which detects both IgM and IgG antibody, and ELISA. The last is increasingly used as a screening test to detect IgG antibody, although some false positives may result.
Differential Diagnosis Primary and secondary syphilis include candidiasis, leukoplakia, hairy leukoplakia, lichen planus, aphthous ulcers, herpetic gingivostomatitis, erythema multiforme, TB, and trauma.
The most effective drug for syphilis is procaine benzyl-penicillin. Doxycycline or erythromycin can be used in patients who are sensitive to penicillin. Follow-up with regular clinical and serologic examinations is necessary for at least 2 years, and contact tracing is recommended.
Tuberculosis
There is a well-known phrase that states, “The more things change, the more they stay the same”. This expression continues to apply to tuberculosis (TB), a widespread infectious disease scourge traced back to the earliest of centuries. As a result of a resurgence of TB cases in the United States during the 1980s, attention refocused on the factors associated with the observed reversal of a previous declining disease trend; transmission modes of Mycobacterium tuberculosis, occupational infection risks associated with health care, and airbome-hazard infection control precautions. Despite dramatic improvements in public health measures associated with M. tuberculosis infection and disease, such as living conditions, nutrition, and antimicrobial chemotherapy, that resulted in an observed dramatic decline in the incidence of TB in the United States and certain other countries during the past century, TB remains a major public health concern for much of the world’s population.
Etiology and pathogenesis
The genus Mycobacterium contains a variety of species, ranging from human pathogens to relatively harmless organisms. As the major cause of TB, a chronic communicable disease, M. tuberculosis is by far the most historically prominent member of this group of bacteria. In addition to their very slow growth on special enriched media, these aerobic slender rods are characterized by their acid-fast staining feature. The unusually high lipid content of the cell wall confers the organisms with an ability to strongly retain a red dye (carbolfuchsin) after treatment with an acid- alcohol solution. This unique structure also allows the bacteria to survive outside a host’s body, suspended in airborne microdroplet nuclei for extended periods of time.
Contrary to a perception believed through the ages, M. tuberculosis is not a highly contagious bacterium. It does not synthesize potent exotoxins or extracellular enzymes, and it is not surrounded by an antiphagocytic capsule. Onset of infection appears to be related to the ability of tubercle bacilli to multiply within host cells and tissues while at the same time resisting host defenses. Infection with M. tuberculosis typically requires prolonged close contact of a susceptible host with an infectious source. The closeness of the contact with aerosolized bacilli and the degree of infec- tivity of the mycobacterial source are the most important considerations for infection. The overwhelming majority of primary human infections involve inhalation of mycobacteria-laden respiratory microdroplets. The diameter of these aerosolized droplets ranges from 1 to 5 microns. Dispersal of M. tuberculosis occurs via these droplets as a result of coughing, sneezing, or even speaking. Microdroplet nuclei are small enough to bypass protective host bronchial mucocilliary defenses, leading to mycobacteria subsequently replicating in both free alveolar spaces and within phagocytic cells. Repeated prolonged exposure to air that has been contaminated by droplets from a person with TB predisposes others to infection. This rationale is illustrated by the fact that people who live in the same home with an infected individual, or close friends or co-workers who routinely breathe the same mycobacteria-contaminated air from an undiagnosed or untreated person with pulmonary TB, have a high risk of acquiring infection. The organisms’ oxygen requirement predisposes the lungs as primary infection sites, with the potential for subsequent dissemination to other tissues. Crossinfection or spread of tubercle bacilli does not result from casual or sporadic exposure.
Onset of clinical disease is characterized by gradual infiltration of neutrophils, macrophages, and T lymphocytes. Distinctive granulomatous TB lesions called tu-
bercles may appear anywhere in the lung parenchyma; however, they are most evident in the periphery. Because TB is the prototype microbial infection for inducing protective cellular immunity, the immunocompetence of the affected host plays a significant role in controlling the extent and severity of resultant disease. It is important to remember that most people infected with M. tuberculosis develop a positive type IV hypersensitive skin test reaction when challenged but do not progress to clinical disease. For those infected individuals who develop clinical symptoms, fatigue, malaise, weight loss, night sweats, and fever are most commonly noted in addition to positive chest radiograph manifestations. Pulmonary manifestations most frequently are chest pain, bloody sputum, and the presence of a prolonged productive cough of greater than 3 weeks’ duration.
Initial mycobacterial infection may progress to several different states depending on the extent of M tuberculosis exposure and resistance of the patient. These include (1) asymptomatic primary tuberculosis, (2) symptomatic primary tuberculosis, (3) progressive primary tuberculosis, and (4) reactivation tuberculosis. A major risk factor for progression of initial infection with tubercle bacilli to more severe disease stages is the absence of an adequate host acquired cellular immune response to mycobacterial antigens. The ability of an infected individual to develop dual cellular and humoral immune responses against M tuberculosis antigens thus greatly influences disease onset and progression.
Asymptomatic Primary Tuberculosis. Individuals may be infected with M. tuberculosis without apparent clinical manifestations. When skin tested, individuals with asymptomatic primary tuberculosis display a positive tuberculin reaction indicating that they have been infected and have developed cell-mediated immunity against the bacteria. This protective immune response prevents the continued multiplication and dissemination of the bacteria, but it does not destroy all of the bacteria present. The remaining bacteria are sequestered within tubercles in the affected tissues and may be the source of bacteria that initiate reactivation tuberculosis.
Symptomatic Primary Tuberculosis. In symptomatic primary tuberculosis, M. tuberculosis is spread via the lymphatics to cause granulomatous inflammation in both the lung periphery and hilar nodes, and it is accompanied by respiratory symptoms. The usual result is one of healing and development of cell-mediated immunity. The Ghon complex, a remnant of this infection, most often occurs in infants and children and is comprised of small calcified lung nodules and lymphadenopathy of the hilar lymph nodes.
Progressive Primary Tuberculosis. A much more serious disease may develop in those individuals who are less resistant to tubercle bacilli. In these patients, microorganisms may spread throughout the body either (1) by means of the blood, resulting in miliary tuberculosis; (2) via the respiratory tissues, inducing a bronchopneumonia; or (3) through the gastrointestinal tract as a result of the organisms being coughed up. In miliary tuberculosis, foci of infection occur in distant organs and tissues but most frequently develop in the meninges, lungs, liver, and renal cortex. Although cell-mediated immunity may develop in some patients, others may not react (anergy) when skin tested with tuberculin protein preparations. Anergic patients have a poor prognosis for recovery and often die without rapid treatment.
Reactivation Tuberculosis. Reactivation tuberculosis occurs in individuals who have developed primary tuberculosis and who are asymptomatic, but who still carry the bacteria within tubercles. These patients exhibit positive tuberculin skin tests and thus demonstrate cellular immunity. Reactivation of disease is thought to be due to the activation of persistent bacteria in the tubercles of a previous infection, which become activated by some alteration in host resistance. Infection is characterized by tubercle formation, caseation, fibrosis, and further extension of the lesion. Progression may advance into a bronchus, leading to cavitation of the lung and secretion of an infectious sputum.
Oral manifestations
Oral manifestations of tuberculosis occur in approximately 3 % of cases involving long-standing pulmonary and/or systemic infection. The bacteria can infect oral tissues and lymph nodes (scrofula). Within the oral cavity, lesions can occur in the soft tissues and supporting bone and in tooth extraction sites, and may even affect the tongue and floor of the mouth.
When reviewing this information, it becomes apparent that progression of infection with tubercle bacilli to more severe disseminated stages occurs in the absence of adequate cellular immunity to infection. Thus, the ability of an infected individual to develop a dual immune response against M. tuberculosis antigens greatly influences disease onset and progression. These crucial protective responses are (1) acquired immunity to infection and (2) development of tuberculin hypersensitivity.
Diagnosis
A diagnosis of infection with M. tuberculosis relies on (1) development of a positive delayed hypersensitivity (tuberculin) skin reaction to purified protein derivative (PPD), a mycobacterial antigen isolated from bacterial cultures, and (2) demonstration of acid-fast mycobacteria in clinical specimens. Information obtained while collecting a patient’s medical history can provide evidence for suspicion of TB.
Treatment
Prior to the advent of antimicrobial chemotherapy, approximately 50 % of persons with active TB died within 2 years after onset of symptoms. Regimens of multiple antibiotics are currently used to treat patients with active TB to ensure tissue penetration and minimize emergence of resistant organisms. General guidelines for appropriate TB chemotherapy include necessity for long-term treatment interval (up to 2 years), initiation of treatment if sputum smear is positive for acid-fast bacilli, and patient compliance (a major factor in determining chemotherapy success).
Isoniazid (INH) is the antimycobacterial therapy cornerstone and is included in all routine drug regimens. People who develop a positive tuberculin skin reaction but do not have active disease, as well as close contacts of patients who develop TB, are placed on INH for 6 months to 1 year.
For treatment of patients with active TB, combinations of three or more drugs are chosen based on the nature and site of disease. In addition to INH, rifampin, pyrazinamide, and ethambutol are the most frequently applied drug combinations unless a specific instance of mycobacterial resistance is noted. Hepatotoxicity is a frequent adverse effect noted with prolonged administration of antimycobacterial chemotherapy.
Unfortunately, a major complication preventing successful elimination of acid- fast organisms in TB patients is non— compliance to the prolonged drug regimens. Patients often notice a substantial decline in symptoms within a few weeks of therapy and prematurely discontinue their medications. Consequently, bacterial strains causing multidrug-resistant tuberculosis (MDR-TB) have emerged and spread throughout the world.
Chemotherapy for tuberculosis: Combination therapy: usually 3—4 drugs to prevent resistance, chosen from the following: isoniazid, rifampin, ethambutol, rifabutin, streptomycin, pyrazinamide; Prolonged therapy — 6 months minimum — indicated for slow growth rate of bacteria, increasing incidence of Mycobacterium tuberculosis drug resistance.
Precancerous diseases of oral mucosa and lips. Risk factors of development of oncologic diseases
The processes, which precede the development of tumor, are called pretumor- ous, and with respect to cancer — precancerous. Precancerous processes differ from
cancer in terms of absence of one or several symptoms, which make it possible to place the diagnosis of cancer.
The development of cancer is contributed by:
• chronic injuries;
• chronic inflammatory processes, accompanied by erosions and ulcers,
• proliferating processes,
• benign tumors.
Depending on frequency transition of cancer from obligatory and facultative diseases precancerous diseases are distinguished.
Obligatory precancerous diseases without treatment for different time periods surely lead to the development of cancer.
Facultative precancerous diseases do not always lead to cancer.
Obligatory precancers include:
• Bowen’s disease,
• verruciform precancer of the red border of lips,
• Manganotti’s abrasive precancerous cheilitis,
• limited precancerous hyperkeratosis of the red border of lips.
Facultative precancers include:
• erosive and verrucosa leukoplakia,
• papillomatosis,
• erosive-ulcerous and hyperkeratosic forms of lichen ruber planus and lupus erythematosis,
• chronic cracks of lips,
• skin hom,
• keratoacanthoma,
• post radiography stomatitis.
Bowen’s disease
Bowen’s disease (morben Bowen). It is potentially most malignant among all precancerous illnesses and is plotted in the concept of cancer in situ. Most frequently the soft palate, uvula, the retromolar region, the tongue are involved.
Clinic. A stricken area is usually one, rarely — two; it is the limited stagnant- red spot with smooth or velvety surface, with small papillary growths. As a result of the atrophy of mucous membrane the center will begin to slightly fall in comparison with the surrounding tissues.
The papillae of the tongue disappear near the lesion, if the lesion is localized in the tongue.
Disease runs an indeterminate time. In certain cases invasive increase rapidly begins, in others — it remains in the stage of cancer “in situ” for years.
Diagnostics. Diagnosis is confirmed by the histopathological study, which reveals the picture of intra-epithelial cancer: the polymorphism of the cells of prickly layer, an increase in the number of mitoses, their irregularity, gigantic and poly- nuclear cells, acanthosis, sometimes hyper— and parakeratosis.
The treatment of Bowen’ s disease consists in the complete removal of stricken areas in the limits of healthy tissues. If it is impossible, short-distance radiation therapy is used.
Verruciform precancer
Verruciform precancer (praecancer of verrucosus). It appears almost exclusively on the red border of the lower lip. It has the type of the half-globular node — with a diameter of 4-10 mm, which is raised on 4-5 mm. On the top the node is covered with the tightly sitting gray fish-scales.
Treatment consists in the complete surgical removal of lesion in the limits of healthy tissues.
Manganotti’s abrasive precancerous cheilitis
Manganotti’s abrasive precancerous cheilitis (cheilitis abrasiva praecancro- sa Manganotti). It is encountered predominantly in men older than 50 years of age. At Manganotti’s cheilitis age-specific trophic changes in the tissues and especially in lower lip are of great importance. In connection with this, in some people in response to the action of different stimuli, the torpid destructive processes are observed. In the pathogenesis of disease metabolic disorder gastrointestinal tract dysfunction, hypovitaminosis A should be considered.
Clinic. The presence of one, rarely two and more erosions of rounded, oval or irregular shapes near the middle of red border of lip are characteristic. The surface of erosion is smooth, clear red. In some patients it is covered with a thin layer of epithelium or the crusts are formed on it. Infiltration of tissues at the base, around the erosion, is not observed. Erosions exist for a long time, sometimes they epithe- lialize, and then they again appear at the same or another place.
Treatment It is necessary, first of all, to eliminate local irritating factors, and also detect and treat associated diseases of other organs and systems. If with a cytological
examination the symptoms of the malignancy of Manganotti’s cheilitis are not revealed, then general and local treatment are carried out before the radical surgical intervention. The use of vitamin A concentrate, nicotinic acid, Nerobol is effective. Locally application of vitamin A concentrate, methyluracil, corticosteroid ointments, solkoseril are prescribed. If conservative treatment within 1 month does not lead to the epithelization of erosion, the surgical removal of stricken area is used.
Circumscribed precancerous hyperkeratosis of the red border of the lips
Circumscribed precancerous hyperkeratosis of the red border of lips (hyperkeratosis praecancrosa circumscripta). Middle-aged men predominate among the patients. Process is localized on the red border of the lower lip, on the side from the centre.
Clinic. The centre of keratinization has a polygonal form, with the size of 5-2 mm. It does not rise above the epithelium, but sometimes it will begin to fall back. Its surface is covered with thin, tightly fastened fish-scales.
Treatment consists in the surgical removal of stricken area in the limits of healthy tissues.
Dermatic horn
Dermatic horn (cornu cutaneum) is limited hyperplasia of the epithelium with the sharply pronounced hyperkeratosis, which in a form and density resembles a hom. It appears on the red border of the lip, more often on the lower one, in people older than 60 years.
Clinic is sufficiently typical. Lesion is a clearly limited centre with the diameter up to 10 mm, from which dirty or brown-gray protrusion of a cone-shaped form with a height not more than 10 mm, rises. A dermatic hom can exist for years, but malignancy at any time can begin. The appearance of inflammation and packing around the base of the hom, strengthening of the intensity of keratinization are the symptoms of malignancy.
Treatment consists in the surgical removal of stricken area in the limits of healthy tissues.
Keratoacantoma
Keratoacantoma (ceratoacantoma) — a benign epidermal tumor, which is most frequently localized on the red border of the lower lip, rarely -— on the tongue.
Clinic. Disease begins with the formation on the lip or the tongue of sulfur- red nodule with the crateriform deepening in the centre, filled with homy masses. Within a month the tumor reaches the maximum size (25 x 10 mm). Most frequently it disappears itself in 6-8 months, and an atrophic pigmented scar is formed on its place or it can be transformed into cancer.
The treatment of keratoacantoma is surgical — removal in the limits of healthy tissues.
Allergic lesions of oral mucosa
Chronic recurrent aphthous stomatitis (RAS)
RAS is a disorder characterized by recurring ulcers confined to the oral mucosa in patients with no other signs of disease. Many specialists and investigators in oral medicine no longer consider RAS to be a single disease but, rather, several pathologic states with similar clinical manifestations. Immunologic disorders, hematologic deficiencies, and allergic or psychological abnormalities have all been implicated in cases of RAS.
RAS affects approximately 20 % of the general population, but when specific ethnic or socioeconomic groups are studied, the incidence ranges from 5 to 50 %. RAS is classified according to clinical characteristics: minor ulcers, major ulcers (Sutton’s disease, periadenitis mucosa necrotica recurrens), and herpetiform ulcers. Minor ulcers, which comprise over 80 % of RAS cases, are less than 1 cm in diameter and heal without scars. Major ulcers, are over 1 cm in diameter and take longer to heal and often scar. Herpetiform ulcers are considered a distinct clinical entity that manifests as recurrent crops of dozens of small ulcers throughout the oral mucosa.
Clinical manifestations
The first episodes of RAS most frequently begin during the second decade of life and may be precipitated by minor trauma, menstruation, upper respiratory infections, or contact with certain foods. The lesions are confined to the oral mucosa and begin with prodromal burning any time from 2 to 48 hours before an ulcer appears. During this initial period, a localized area of erythema develops. Within hours, a small white papule forms, ulcerates, and gradually enlarges over the next 48 to 72 hours. The individual lesions are round, symmetric, and shallow (similar to viral ulcers), but no tissue tags are present from ruptured vesicles (this helps
to distinguish RAS from disease with irregular ulcers such as EM, pemphigus, and pemphigoid). Multiple lesions are often present, but the number, size, and frequency of them vary considerably. The buccal and labial mucosae are most commonly involved. Lesions are less common on the heavily keratinized palate or gingiva. In mild RAS, the lesions reach a size of 0.3 to 1.0 cm and begin healing within a week. Healing without scarring is usually complete in 10 to 14 days.
Most patients with RAS have between two and six lesions at each episode and experience several episodes a year. The disease is an annoyance for the majority of patients with mild RAS, but it can be disabling for patients with severe frequent lesions, especially those classified as major aphthous ulcers. Patients with major ulcers develop deep lesions that are larger than 1 cm in diameter and may reach 5 cm. Large portions of the oral mucosa may be covered with large deep ulcers that can become confluent. The lesions are extremely painful and interfere with speech and eating. Many of these patients continually go from one clinician to another, looking for a “cure”. The lesions may last for months and sometimes be misdiagnosed as squamous cell carcinoma, chronic granulomatous disease, or pemphigoid. The lesions heal slowly and leave scars that may result in decreased mobility of the uvula and tongue and destruction of portions of the oral mucosa. The least common variant of RAS is the herpetiform type, which tends to occur in adults. The patient presents with small punctate ulcers scattered over large portions of the oral mucosa.
Diagnosis
RAS is the most common cause of recurring oral ulcers and is essentially diagnosed by exclusion of other diseases. A detailed history and examination by a knowledgeable clinician should distinguish RAS from primary acute lesions such as viral stomatitis or from chronic multiple lesions such as pemphigoid, as well as from other possible causes of recurring ulcers, such as connective tissue disease, drug reactions, and dermatologic disorders. The history should emphasize symptoms of blood dyscrasias, systemic complaints, and associated skin, eye, genital, or rectal lesions. Laboratory investigation should be used when ulcers worsen or begin past the age of 25 years.‘Biopsies are only indicated when it is necessary to exclude other diseases, particularly granulomatous diseases such as Crohn’s disease or sarcoidosis.
Patients with severe minor aphthae or major aphthous ulcers should have known associated factors investigated, including connective-tissue diseases and abnormal levels of serum iron, folate, vitamin B12, and ferritin. Patients with abnormalities in these values should be referred to an internist to rule out malabsorp' tion syndromes and to initiate proper replacement therapy. The clinician may also choose to have food allergy or gluten sensitivity investigated in severe cases resistant to other forms of treatment. HIV-infected patients, particularly those with CD4 counts below 100/mm3, may develop major aphthous ulcers.
Treatment
Medication prescribed should relate to the severity of the disease. In mild cases with two or three small lesions, use of a protective emollient such as Orabase or Zi- lactin is all that is necessary. Pain relief of minor lesions can be obtained with use of a topical anesthetic agent or topical diclofenac, an NSAID frequently used topically after eye surgery.
In more severe cases, the use of a high-potency topical steroid preparation, such as fluocinonide, betamethasone or clobetasol, placed directly on the lesion shortens healing time and reduces the size of the ulcers. The effectiveness of the topical steroid is partially based upon good instruction and patient compliance regarding proper use. The gel can be carefully applied directly to the lesion after meals and at bedtime two to three times a day, or mixed with an adhesive such as Orabase prior to application. Larger lesions can be treated by placing a gauze sponge containing the topical steroid on the ulcer and leaving it in place for 15 to 30 minutes to allow for longer contact of the medication. Other topical preparations that have been shown to decrease the healing time of RAS lesions include amlexanox paste and topical tetracycline, which can be used either as a mouth rinse or applied on gauze sponges. Intralesional steroids can be used to treat large indolent major RAS lesions. It should be emphasized that no available topical therapy decreases the onset of new lesions. In patients with major aphthae or severe cases of multiple minor aphthae not responsive to topical therapy, use of systemic therapy should be considered. Drugs that have been reported to reduce the number of ulcers in selected cases of major aphthae include colchicine, pentoxifylline, dapsone, short bursts of systemic steroids, and thalidomide. Each of these drugs has the potential for side effects, and the clinician must weigh the potential benefits versus the risks. Thalidomide has been shown to reduce both the incidence and severity of major RAS in both HIV-positive and HIV-negative patients, but this drug must be used with extreme caution in women during childbearing years owing to the potential for severe life-threatening and deforming birth defects.
Erythema multiforme
Erythema multiforme (EM) is an acute inflammatory disease of the skin and mucous membranes that causes a variety of skin lesions — hence the name “multiforme”. The oral lesions, typically inflammation accompanied by rapidly rupturing vesicles and bullae, are often an important component of the clinical picture and are occasionally the only component. Erythema multiforme may occur once or recur, and it should be considered in the diagnosis of multiple acute oral ulcers whether or not there is a history of similar lesions. There is also a rare chronic form of EM. EM has several clinical presentations: a milder self-limiting form and severe life-threatening forms that may present as either Stevens—Johnson syndrome or toxic epidermal necrolysis (TEN).
Etiology. EM is an immune-mediated disease that may be initiated either by deposition of immune complexes in the superficial microvasculature of skin and mucosa, or cell-mediated immunity.
The most common triggers for episodes of EM are herpes simplex virus and drug reactions. The drugs most frequently associated with EM reactions are oxi- cam nonsteroidal antiinflammatory drugs (NSAIDs); sulfonamides; anticonvulsants such as carbamazepine, phenobarbital, and phenytoin; trimethoprim-sulfonamide combinations, allopurinol, and penicillin. A majority of the severe cases of Stevens—Johnson syndrome or TEN are caused by drug reactions.
Clinical manifestations
General Findings. EM is seen most frequently in children and young adults and is rare after age 50 years. It has an acute or even an explosive onset; generalized symptoms such as fever and malaise appear in severe cases. A patient may be asymptomatic and in less than 24 hours have extensive lesions of the skin and mucosa. EM simplex is a self-limiting form of the disease and is characterized by macules and papules 0.5 to 2 cm in diameter, appearing in a symmetric distribution.
The most common cutaneous areas involved are: hands, feet, and extensor surfaces of the elbows and knees. The face and neck are commonly involved, but only severe cases affect the trunk. Typical skin lesions of EM may be nonspecific macules, papules, and vesicles. More typical skin lesions contain petechiae in the center of the lesion. The pathognomonic lesion is the target or iris lesion, which consists of a central bulla or pale clearing area surrounded by edema and bands of erythema.
The more severe vesiculobullous forms of the disease, Stevens—Johnson syndrome and TEN, have a significant mortality rate. EM is classified as Stevens— Johnson syndrome when the generalized vesicles and bullae involve the skin, mouth, eyes, and genitals.
The most severe form of the disease is TEN, (tone epidermal neurolysis), which is usually secondary to a drug reaction and results in sloughing of skin and mucosa in large sheets. Morbidity, which occurs in 30 to 40 % of patients, results from secondary infection, fluid and electrolyte imbalance, or involvement of the lung, liver, or kidneys. Patients with this form of the disease are most successfully managed in bum centers, where necrotic skin is removed under general anesthesia and healing takes place under sheets of porcine xenografts.
Oral lesions commonly appear along with skin lesions in approximately 70 % of EM patients. In some cases, oral lesions are the predominant or single site of disease. When the oral lesions predominate and no target lesions are present on the skin, EM must be differentiated from other causes of acute multiple ulcers, especially primary herpes simplex infection. This distinction is important because corticosteroids may be the treatment of choice in EM, but they are specifically contraindicated in primary herpes simplex infections. When there are no skin lesions and the oral lesions are mild, diagnosis may be difficult and is usually made by exclusion of other diseases. Cytologic smears and virus isolation may be done to eliminate the possibility of primary herpes infection. Biopsy may be performed when acute pemphigus is suspected. The histologic picture of oral EM is not considered specific, but the finding of a perivascular lymphocytic infiltrate and epithelial edema and hyperplasia is considered suggestive of EM. The diagnosis is made on the basis of the total clinical picture, including the rapid onset of lesions. The oral lesions start as bullae on an erythematous base, but intact bullae are rarely seen by the clinician because they break rapidly into irregular ulcers. Viral lesions are small, round, symmetric, and shallow, but EM lesions are larger, irregular, deeper, and often bleed. Lesions may occur anywhere on the oral mucosa with EM, but involvement of the lips is especially prominent, and gingival involvement is rare. This is an important criterion for distinguishing EM from primary herpes simplex infection, in which generalized gingival involvement is characteristic.
In full-blown clinical cases, the lips are extensively eroded, and large portions of the oral mucosa are denuded of epithelium. The patient cannot eat or even swallow and drools blood-tinged saliva. Within 2 or 3 days the labial lesions begin to crust. Healing occurs within 2 weeks in a majority of cases, but, in some severe cases, extensive disease may continue for several weeks.
Treatment. Mild cases of oral EM may be treated with supportive measures only, including topical anesthetic mouthwashes and a soft or liquid diet. Moderate to severe oral EM may be treated with a short course of systemic corticosteroids in patients without significant contraindications to their use. Systemic corticosteroids should only be used by clinicians familiar with the side effects, and, in each case, potential benefits should be carefully weighed against potential risks. Young children treated with systemic steroids for EM appear to have a higher rate of complications than do adults, particularly gastrointestinal bleeding and secondary infections.
Adults treated with short-term systemic steroids have a low rate of complications and a shorter course of EM. The protein-wasting and adrenal-suppressive effects of systemic steroids are not significant when used short-term, and the clinical course of the disease may be shortened. An initial dose of 30 mg/d to 50 mg/d of prednisone or methylprednisolone for several days, which is then tapered, is helpful in shortening the healing time of EM, particularly when therapy is started early in the course of the disease. It should be noted that the efficacy of this treatment has not been proven by controlled clinical trials and is controversial.
Patients with severe cases of recurrent EM have been treated with dapsone, aza- thioprine, levamisole, or thalidomide. EM triggered by progesterone, also referred to as autoimmune progesterone dermatitis and stomatitis, has been oophorectomy has been necessary to cure the disorder. Antiherpes drugs such as acyclovir or vala- cyclovir can be effective in preventing susceptible patients from developing herpes- associated EM, if the drug is administered at the onset of the recurrent HS V lesion. Prophylactic use of antiherpes drugs is effective in preventing frequent recurrent episodes of HSV-associated EM. Systemic steroids are recommended for management of Stevens-Johnson syndrome and are considered life saving in severe cases.
Pemphigus vulgaris
PV is the most common form of pemphigus, accounting for over 80 % of cases. The underlying mechanism responsible for causing the intraepithelial lesion of PV is the binding of IgG autoantibodies to desmoglein 3, a transmembrane glycoprotein adhesion molecule present on desmosomes.
Typical lesions of recurrent intraoral herpes simplex virus infection in patients with normal immunity are clusters of small vesicles and ulcers on the heavily keratinized oral mucosa. Ulcerative, Vesicular, and Bullous Lesions gus foliaceus, but these antibodies are also detected in patients with long-standing PV. Evidence for the relationship of the IgG autoantibodies to PV lesion formation includes studies demonstrating the formation of blisters on the skin of mice after passive transfer of IgG from patients with PV. The mechanism by which antidesmoglein antibodies cause the loss of cell-to-cell adhesion is controversial. Some investigators believe that binding of the PV antibody activates proteases, whereas more recent evidence supports the theory that the PV antibodies directly block the adhesion function of the desmogleins.
The separation of cells, called acantholysis, takes place in the lower layers of the stratum spinosum. Electron microscopic observations show the earliest epithelial changes as a loss of intercellular cement substance; this is followed by a
widening of intercellular spaces, destruction of desmosomes, and finally cellular degeneration. This progressive acantholysis results in the classic suprabasilar bulla, which involves increasingly greater areas of epithelium, resulting in loss of large areas of skin and mucosa.
Pemphigus has been reported coexisting with other autoimmune diseases, particularly myasthenia gravis. Patients with thymoma also have a higher incidence of pemphigus. Several cases of pemphigus have been reported in patients with multiple autoimmune disorders or those with neoplasms such as lymphoma. Death occurs most frequently in elderly patients and in patients requiring high doses of corticosteroids who develop infections and bacterial septicemia, most notably from Staphylococcus aureus.
Clinical Manifestations. The classical lesion of pemphigus is a thin-walled bulla arising on otherwise normal skin or mucosa. The bulla rapidly breaks but continues to extend peripherally, eventually leaving large areas denuded of skin. A characteristic sign of the disease may be obtained by application of pressure to an intact bulla. In patients with PV, the bulla enlarges by extension to an apparently normal surface. Another characteristic sign of the disease is that pressure to an apparently normal area results in the formation of a new lesion. This phenomenon, called the Nikolsky sign, results from the upper layer of the skin pulling away from the basal layer. The Nikolsky sign is most frequently associated with pemphigus but may also occur in epidermolysis bullosa.
Some patients with pemphigus develop acute fulminating disease, but, in most cases, the disease develops more slowly, usually taking months to develop to its fullest extent.
Oral Manifestations. Eighty to ninety percent of patients with pemphigus vulgaris develop oral lesions sometime during the course of the disease, and, in 60 % of cases, the oral lesions are the first sign. The oral lesions may begin as the classic bulla on a noninflamed base; more frequently, the clinician sees shallow irregular ulcers because the bullae rapidly break. A thin layer of epithelium peels away in an irregular pattern, leaving a denuded base. The edges of the lesion continue to extend peripherally over a period of weeks until they involve large portions of the oral mucosa. Most commonly the lesions start on the buccal mucosa, often in areas of trauma along the occlusal plane. The palate and gingiva are other common sites of involvement.
It is common for the oral lesions to be present up to 4 months before the skin lesions appear. If treatment is instituted during this time, the disease is easier to control, and the chance for an early remission of the disorder is enhanced. Frequently, however, the initial diagnosis is missed, and the lesions are misdiagnosed
as herpes infection or candidiasis. Zegarelli and Zegarelli studied 26 cases of intraoral PV. The average time from onset of the disease to diagnosis was 6-8 months. They also noted that several patients had coexisting candidiasis, which sometimes masked the typical clinical picture of the pemphigus lesions. There is also a subgroup of pemphigus patients whose disease remains confined to the oral mucosa. These patients often have negative results on direct immunofluorescence (DIF). If a proper history is taken, the clinician should be able to distinguish the lesions of pemphigus from those caused by acute viral infections or erythema multiforme because of the acute nature of the latter diseases. It is also important for the clinician to distinguish pemphigus lesions from those in the RAS category. RAS lesions may be severe, but individual lesions heal and recur. In pemphigus, the same lesions continue to extend peripherally over a period of weeks to months. Lesions of pemphigus are not round and symmetric like RAS lesions but are shallow and irregular and often have detached epithelium at the periphery. In early stages of the disease, the sliding away of the oral epithelium resembles skin peeling after a severe sunburn. In some cases, the lesions may start on the gingiva and be called desquamative gingivitis. It should be remembered that desquamative gingivitis is not a diagnosis in itself; these lesions must be biopsied to rule out the possibility of PV as well as bullous pemphigoid,mucous membrane pemphigoid, and erosive lichen planus.
Laboratory Tests. PV is diagnosed by biopsy. Biopsies are best done on intact vesicles and bullae less than 24 hours old; however, because these lesions are rare on the oral mucosa, the biopsy specimen should be taken from the advancing edge of the lesion, where areas of characteristic suprabasilar acantholysis may be observed by the pathologist. Specimens taken from the center of a denuded area are nonspecific histologically as well as clinically. Sometimes several biopsies are necessary before the correct diagnosis can be made. If the patient shows a positive Nikolsky sign, pressure can be placed on the mucosa to produce a new lesion; biopsy may be done on this fresh lesion.
A second biopsy, to be studied by DIF, should be performed whenever pemphigus is included in the differential diagnosis.
Treatment. An important aspect of patient management is early diagnosis, when lower doses of medication can be used for shorter periods of time to control the disease. The mainstay of treatment remains high doses of systemic corticosteroids, usually given in dosages of 1 to 2 mg/kg/d. When steroids must be used for long periods of time, adjuvants such as azathioprine or cyclophosphamide are added to the regimen to reduce the complications of long-term corticosteroid therapy. Prednisone is used initially to bring the disease under control, and, once this is achieved, the dose of prednisone is decreased to the lowest possible maintenance levels. Patients
with only oral involvement also may need lower doses of prednisone for shorter periods of time, so the clinician should weigh the potential benefits of adding adjuvant therapy against the risks of additional complications such as blood dyscrasias, hepatitis, and an increased risk of malignancy later in life. There is no one accepted treatment for pemphigus confined to the mouth, but one 5-year follow-up study of the treatment of oral pemphigus showed no additional benefit of adding cyclophosphamide or cyclosporine to prednisone versus prednisone alone, and it showed a higher rate of complications in the group taking the immunosuppressive drug.
Most studies of pemphigus of the skin show a decreased mortality rate when adjuvant therapy is given along with prednisone. One new immunosuppressive drug, mycophenolate, has been effective when managing patients resistant to other adjuvants. The need for systemic steroids may be lowered further in cases of oral pemphigus by combining topical with systemic steroid therapy, either by allowing the prednisone tablets to dissolve slowly in the mouth before swallowing or by using potent topical steroid creams. Other therapies that have been reported as beneficial are parenteral gold therapy, dapsone, tetracycline, and plasmapheresis.
Plasmapheresis is particularly useful in patients refractory to corticosteroids. A therapy described by Rook and colleagues involves administration of 8-methoxyp- soralen followed by exposure of peripheral blood to ultraviolet radiation.
Pemphigus vegetans
Pemphigus vegetans, which accounts for 1 to 2 % of pemphigus cases, is a relatively benign variant of pemphigus vulgaris because the patient demonstrates the ability to heal the denuded areas. Two forms of pemphigus vegetans are recognized: the Neumann type and the Hallopeau type. The Neumann type is more common, and the early lesions are similar to those seen in pemphigus vulgaris, with large bullae and denuded areas. These areas attempt healing by developing vegetations of hyperplastic granulation tissue. In the Hallopeau type, which is less aggressive, pustules, not bullae, are the initial lesions. These pustules are followed by verrucous hyperkeratotic vegetations.
Biopsy results of the early lesions of pemphigus vegetans show suprabasilar ac- antholysis. In older lesions, hyperkeratosis and pseudoepitheliomatous hyperplasia become prominent. Immunofluorescent study shows changes identical to those seen in PV. Oral Manifestations. Oral lesions are common in both forms of pemphigus vegetans and may be the initial sign of disease. Gingival lesions may be lace-like ulcers with a purulent surface on a red base or have a granular or cobblestone appearance. Oral lesions that are associated with inflammatory bowel disease and
resemble pemphigus vegetans both clinically and histologically are referred to by some authors as pyostomatitis vegetans.
Treatment. Treatment is the same as that for PV.
Lichen ruber planus
Lichen ruber planus (Lichen ruber planus) is the chronic disease, which is manifested on the skin and the mucous membranes by formation of the keratinized papules.
LRP oral mucosa is usually encountered in people of middle age, predominantly in women. Very rarely this illness can be found at younger age, and also in children.
Elements of lesion.
Separate papules which appear on the skin are more often miliary. Their base is slightly infiltrated, round, oval, and sometimes elongated. Here at first the papules have lusterless colour, then they turn pink, reddish and even lilac-violet; sometimes long-existing papule turn brown. Since the papules are comification, they slightly rise above the surrounding skin.
The favourite places of the precipitations of papules LRP on the skin are flexible surfaces. On the hands — this is the region of radiocarpal joint. The development of disease is possible on mucosa membrane in different parts of gastrointestinal tract.
LRP of oral mucosa has predominantly two localizations:
• The most typical is the distal part of the cheek or the pear-shaped region, where the polygonal papules, after merging between themselves, form a figure in the form of fem leaves or grid; they are clearly defined and can be palpated;
• The tongue (dorsal and lateral surface), in which the signs of disease are represented very diversely: the polygonal knots, which form an area either covered with scar-like strips as grids, the atrophic sections of oral mucosa, or hypertrophic papules.
Treatment.
The complex therapy LRP includes two groups of the measures:
1. general action;
2. action directed to the LRP centre.
The general directions of the therapy of all LRP forms are: the liquidation of keratosis and inflammation, and the normalization of the process of callusing the epithelium, and also the elimination of intra— and para-focal complications (erythema, erosions, bubbles, welding dribbles, ulcers).
Local treatment consists in the elimination of the irritating factors.
Changes in the oral mucosa at diseases of internal organs and systems
Changes in the oral mucosa at diseases of gastrointestinal tract
Changes in the tongue. They are the most typical at diseases of gastrointestinal tract. Among these signs the furred tongue is most frequently revealed. The disturbance of the process of comification and destruction of epithelial cells in the tongue papillae, as a result of the neurotrophic disorders, play an important role in the formation of fur on the tongue. The nature of food, the composition of microflora, the oral hygiene influence the accumulation of fur. If the epithelium detachment is not observed, the keratinized cells remain, dead leukocytes and microorganisms of saliva are joined and form fur. In this case the favorable conditions for multiplication of microorganisms are created, in particular, a significant amount of fungi is formed. All of this is the basis of fur. Fur is revealed with gastritis, stomach ulcer and duodenal ulcer, new formations in the stomach and other illnesses.
Edema of the tongue is the second sign of gastrointestinal diseases. It does not cause subjective sensations in patient. Edema of the tongue is observed in case of chronic bowel diseases, which is explained by the disturbance of the sucking ability in the gut and gut barrier function. The changes in the different groups of the papillae of the tongue are observed at diseases of gastrointestinal tract. Depending on their state hyper— and hypoplastic glossitis are distinguished.
Hyperplastic glossitis is observed in patients in case of gastritis with increased acidity. It is accompanied by the hypertrophy of papillae, presence of fur, a slight increase in size of the tongue as a result of edema.
Hypoplastic glossitis is characterized by the atrophy of papillae, sometimes sharply expressed, in consequence of which it become varnished, with bright spots and strips. The atrophy of the tongue papillae causes the sensation of burning, tingling, pain when eating. Such changes in the tongue papillae are observed in case of gastritis with lowered secretion, ulcer, gastroenteritis, biliary tract disease.
The intensive exfoliation of the epithelium of the tongue is fairly often observed at diseases of gastrointestinal tract.
Changes of oral mucosa. The most frequent manifestation of the disease of gastrointestinal tract is a change in colour of oral mucosa. The catarrhal stomatitis is observed at hyperacidic and normacidic gastritis, ulcer, enterocolitis. Characteristic pigmentation of oral mucosa occurs in case of liver disease: entire mucosa turns pink, and the soft palate turns yellowish.
The treatment of changes of oral mucosa in case of digestive system diseases is symptomatic. At the same time, it provides for the normalization of the function of these organs, hyposensitizing therapy, vitamin therapy (groups B, C, A, PP), and oral cavitysanitation.
Lesions of the oral mucosa at cardiovascular pathology
Changes of oral mucosa at cardiovascular diseases depend on the degree of insufficiency of blood circulation, state of vascular wall, etc.
Cyanosis of oral mucosa, lips and the tongue of bright red or crimson color are characteristic for the acute period of myocardial infarction.
The appearance of trophic changes of oral mucosa, up to the formation of ulcers, is observed predominantly in patients with the decompensated defects of heart and the disturbance of blood circulation of III, sometimes II degree. Trophic ulcers are localized predominantly in the rear of the mouth, on the cheek mucosa, alveolar branch, on the tongue, on the mucous a pear-shaped area, etc.
Ulcers have different sizes (2-5 mm and more). They are covered with pale gray fur with the fetid smell; it is sharply painful when touching and eating. The inflammatory reaction in the surrounding tissues is absent.
The treatment of such changes of oral mucosa provides for the liquidation of the insufficiency of blood circulation in combination with the local symptomatic therapy;
Changes in the oral mucosa at endocrine diseases
Diabetes mellitus. The most characteristic changes in the oral cavity are xerostomia, catarrhal stomatitis and glossitis, fungal stomatitis, mycotic perleche, paresthesias of oral mucosa, trophic disorders, Lichen ruber planus.
Dentist conducts the treatment of a patient together with the endocrinologist- The symptomatic treatment is prescribed with the expressed changes in the oral cavity taking into account their manifestation.
Myxedema is developed with the insufficiency of the function of the thyroid gland. The face of patient takes the unique form: lips and nose are thickened, upper
eyelids are sharply edematic, and facial expression is indifferent. In patients anemia, edema and dryness of oral mucosa are observed. Myxedema is accompanied by a marked increase of the tongue, which is sometimes not placed in the oral cavity, an increase of the lips, gums.
Dentist conducts the sanitation of the oral cavity and symptomatic treatment if necessary.
Pregnancy gingivitis is an inflammation of gums, which first appears during pregnancy or is exacerbated by pregnancy. The development of the disease is connected with restoring of hormonal balance during this period. In the first half of pregnancy the catarrhal gingivitis is noted. In the second half — the course of disease is heavy, with the development of proliferating process in the gums. In the initial stage of gingivitis the gingival edge becomes clear red, swells, bleeds easily. Gradually the affected gum becomes dark red, cyanotic, increases and with the presence of local stimuli the hypertrophic gingivitis develops. Hypertrophic gingivitis in pregnancy tends to polypous growth of separate papillae. Sometimes false epulis develop. The hypertrophied gum covers the entire dental crown, bleeds easily.
Treatment. The local treatment of pregnancy gingivitis is conducted through the principles of the treatment of catarrhal or hypertrophic gingivitis.
Itsenko-Cushing disease. The oral mucosa in such patients is edematic, the imprints of teeth on the tongue and the cheeks are observed. Appearing trophic disorders lead to the appearance of erosions and ulcers which are characterized by a prolonged course. Candidiasis is frequently observed.
Treatment is carried out together with the endocrinologist. The sanitation of the oral cavity and symptomatic therapy depending on clinical manifestations is indicated.
Addison’s disease is caused by curtailment in production of hormones of the adrenal cortex. The most characteristic feature of the disease is the specific pigmentation of the skin and oral mucosa. The changes in the mucous membrane of the oral cavity in case of diseases of internal organs and systems are: small spots or bluish, grayish black strips. Patients do not subjectively feel it. Changes in the mouth and on the skin appear as a result of the deposit of the large number of melanin.
Manifestations on oral mucosa with the diseases of the blood and hematopoietic organs
Iron-deficiency (hypochromic) anemia (chlorosis). Patients with early chlorosis complain about the disturbance of gustatory senses, sense of smell, reduction in appetite, nausea. The oral mucosa is without the noticeable disturbances, except for color change — it becomes pale. All symptoms are more expressed with late chlorosis. Patients complain about painful sensations in the tongue and oral mu-
cosa when eating sour or spicy food, dryness in the oral cavity, paresthesia (burning, tingling, prickling and bursting the tongue open), and the presence of angular heilitis.
The clinical picture of hypochromic anemia is multiple lesions of carious teeth, their increased abrasion, and loss of the natural luster of enamel. Mucosa membrane of lips, cheeks and gums is pale, edematic. The tongue is edematic, papillae are atrophied, especially in its front part. It becomes clear red and smooth, as if polished, deep folds appear. Sometimes hemorrhages and cracks in the angles of the mouth are observed.
Treatment. The symptomatic therapy of manifestations on mucous membrane is prescribed.
Hypoplastic anemia appears under the action of the exogenous physical (irradiation) and chemical factors, and drugs as well as endogenous aplasia of bone marrow. On the background of particularly pale oral mucosa different heavy hemorrhages appear. Interdental papillae are edematic, cyanotic, sometimes bleeding, deep parodontal pockets are revealed. On oral mucosa, besides petechiae, also erosions, ulcers, necrotic sections are observed.
Treatment. Dentist conducts the symptomatic treatment of the manifestations of hypoplastic anemia.
B12 — folate deficient anemia (malignant anemia, pernicious anemia, Addison — Birmera disease) is characterized by the disturbance of erythropoiesis. The clinical picture of disease consists of the triad: the dysfunction of the gastrointestinal tract, hemopoietic and nervous systems. One of the early symptoms of the disease is the pallor of the skin and oral mucosa with a yellowish tint. Sometimes on oral mucosa petechial hemorrhages are observed. The most characteristic lesion of oral mucosa in case of malignant anemia is hunter’s glossitis. The back of the tongue in this case takes the form of the smooth, bright, polished surface as a result of the atrophy of mushroom-shaped filamentary papillae, thinning of epithelium and atrophy of muscles. Painful, sharply limited strips and spots of clear red color of inflammatory nature appear at the back and the tip of the tongue.
Treatment is carried out in the hematology clinics. Locally symptomatic treatments, sanitation of oral cavity are carried out.
Leucosis is the malignant disease of the hemopoietic organs, which appears as a result of progressive cellular hyperplasia in the hemopoietic organs, when the processes of cellular division (proliferation) prevail above the processes of ripening (differentiation). Pathomorphological substratum of disease is leukemia blast cells, which correspond to primordial elements of one of the hematopoietic lineage.
The clinical picture of acute leucosis determines 4 leading syndromes: hem- orrhagic, hyperplastic, anaemic and intoxicating. Hemorrhagic syndrome is mani-
fested in the form of petechiae, ecchymosis, hematomas on the skin and mucous membrane, or the profuse bleedings.
In the oral cavity the most characteristic are: acute bleeding of gums, presence of hemorrhages on mucous membrane of cheeks along the line of the joining of teeth, in the tongue, the palate. Severe hemorrhages and hematomas sometimes are revealed. Hyperplastic processes are manifested in the increase of the lymph nodes, liver, spleen, tonsils. Frequently hyperplasia is combined with ul- ceronecrotic changes in the gums. Furthermore, necroses are revealed also in the tonsils, the pear-shaped area and other parts of oral mucosa. Its tendency toward the propagation in the adjacent sections is the special feature of necrotic process in case of sharp leucosis, in consequence of which the unlimited ulcers of irregular outlines, covered with gray necrotic fur appear. Reactive changes around the ulcer are absent or are weakly expressed. The development of ulceronecrotic processes in the oral cavity is connected with sharp reduction in the resistibility of tissues caused by reduction in the phagocytic activity of leukocytes and immune properties of blood serum.
Patients with acute leucosis complain about pain in the intact teeth and the jaws (together with pain in other bones), which is explained by the direct lesion of the bones in case of the leukemic process.
Treatment is conducted in the hematology hospitals. The treatment of leukosis stomatitis is symptomatic. The extraction of teeth is contraindicated.
The chronic leucosis appear more rarely than acute, development is more favorable; course is prolonged.
Chronic myeloleukemia passes two stages: benign (lasts several years) and malignant (terminal), which lasts for 3—6 months. The basic sign of chronic myeloleukemia in the oral cavity are hemorrhagic manifestations, but with considerably smaller intensity, than in case of acute leucosis. Bleeding of gums appears not spontaneously, but only with the traumatization, the removal of teeth. In the period of excerbation the ulceronecrotic lesions of oral mucosa are observed.
Chronic lymphoid leukosis is characterized by slow beginning and prolonged latent course.
In the initial stage of disease an increase in groups of lymph nodes is observed. At the developed stage the generalized increase of lymph nodes is observed, the pallor of the skin and the mucous membranes, leukemic infiltrations of gums, the tongue, and hyperplasia of interdental papillae appear. Sometimes the growth of gingival edge reaches the level of the joining of teeth.
Treatment is conducted in the hematology departments. Local treatment consists in care of the oral cavity, full-fledged sanitation, symptomatic therapy.
Agranulocytosis is a syndrome, which is characterized by the significant decrease in the number or absence of neutrophilic granulocytes in the peripheral blood. Ulceronecrotic process in the lips, the gums, the tongue, mucous membrane of cheeks and other sections develop. Ulceronecrotic process can spread into the gullet. The absence of the inflammatory reaction of tissues around the centre of necrosis is important for diagnostics. Frequently necrotic process is combined with candidiasis.
Treatment is conducted in the hematology departments. Local treatment is symptomatic; it includes the antiseptic treatment of oral cavity, anesthetization, removal of necrotic tissues, and prescription of the preparations, which stimulate regeneration.
Erythremiya (polycythemia, the Vaquez’ disease)
Erythremiya appears at the age of 40—60 years, predominantly in men.
Disease begins unnoticeably, and develops slowly. Increased fatigue, bleeding of gums, hemorrhages from the nose are noted. Characteristic symptom for patients is dark-cherry polycythemia of oral mucosa. Lips, the tongue, buccal mucosa are clear red because of the increased content of reduced hemoglobin in the capillaries. Mucous membrane in the region of alveolar branches is friable, with the cyanotic tint; when pressing bleeds easily, interdental papillae are hyperemized, and of dark- cherry colour. Expressive color boundary — cyanosis of soft palate and pale color of hard palate (Cooperman’s symptom) is characteristic. The itching of the skin and paresthesia of oral mucosa due to the increased filling of vessels and the irritation of the interoceptors of capillaries by the blood is possible.
Treatment is conducted by hematologist, making periodic bloodlettings and using the cytostatic therapy with radioactive phosphorus or mielosan.
Thrombocytopenic purpura (Verlgof disease)
The basic clinical symptom of disease is hemorrhages from the skin and oral mucosa, as well as nose and gums, that appear spontaneously or under the effect of the insignificant injury. In general in case of thrombocytopenic purpura the oral mucosa is pale, edematic, atrophied; the thinning of epithelium, erosions or ulcers form.
Treatment is conducted in the hematology departments.
Changes in the oral mucosa at hypo— and avitaminoses
Hypovitaminosis C
The insufficiency of vitamin C is always manifested by changes in the oral cav- ity. Scorbutic stomatitis is one of the earliest and frequent symptoms of the disease. Three stages of scorbutic stomatitis are distinguished:
1. scorbutic stomatopatia — the initial stage;
2. scorbutic reparative stomatitis — the developed stage;
3. scorbutic ulcerous stomatitis — the complicated stage.
Initial stage is characterized by expressed gingivitis on the background of pale anemic oral mucosa: gum becomes infiltrated, gingival edge acquires dark red color, and bleeds easily. Sometimes single, scattered petechia in gum and oral mucosa is observed. Simultaneously petechiae can be revealed on the extremities, in the shin region. Patients complain about general weakness, sleepiness, rheumatic pain in extremities, headache, and rapid fatigue. Initial stage is frequently accompanied by iron-deficiency anemia.
The developed stage of the disease is characterized by the significant inflammation of gums. Gum is sharply edematic, enlarged, and friable; it covers a significant part of the dental crowns. Gingival edge acquires cyanotic tint, it bleeds considerably when pressing. On the edge of gingival papillae the blood clots are frequently accumulated. On oral mucosa the plural petechiae, ecchimozis are observed. The tongue is furred, swells sharply, and the teeth imprints on its edges are observed. Teeth are loosening.
Petechiae, ecchymozis and massive hemorrhages are observed on the mucous membrane of cheeks, palate and in different parts of body. The general state of patients deteriorates, they become adynamic, the face is pale with the earthen tint.
The third, complicated stage of the disease appears with the connection of secondary fixsospirillary infection, in consequence of which scorbutic ulcerous stomatitis develops. The granulations grown on the gingival edge reach the cutting edge or the occlusal surface of teeth; areas of necrosis and pitting appear on the gums. Gums bleed intensively; they are covered with necrotic fur, with the fetid smell. Ulcerous process extends to tongue, cheeks, lips, hard and soft palate. Teeth are loosening and fall out. The general state of patients is extremely heavy. Without the treatment the disease can end lethally.
Treatment. At the initial stage of the disease with correct treatment under the dispensary conditions scorbutic gingivitis disappears in 5-7 days. At the developed and complicated stages of the disease patients subject to hospitalization.
Local treatment: the sanitation of oral cavity is indicated, careful oral hygiene, removal of dental calculus and plaque, irrigation of the oral cavity by the dilute solution of potassium permanganate, the solution of citral, 1 % solution of galaskorbin.
Hypovitaminosis A
Vitamin A (retinol) is of great importance in the processes of growth and devel- °pment of organism; it regulates the processes of ripening and keratinization of the epithelium, increases resistance of oral mucosa to the action on it of different traumatic and irritating factors, ensures the normal functioning of the organ of vision, favors the normal functioning of salivary and sweat glands. The clinical manifestations of hypovitaminosis are caused by reduction in the barrier properties of the skin and oral mucosa, the disruption of the normal differentiation of epithelial tissues. At hypovitaminosis A oral mucosa is pale, turbid, dry, loses its characteristic luster. On mucous membrane of cheeks, the hard and soft palate the whitish stratifications, which resemble the mild form of leukoplakia appear. Keratinization of epithelium of the excretory ducts of salivary glands occurs. This leads to a decrease in secretion of saliva — hyposalivation.
Treatment — products rich in vitamin A (butter, milk, egg yolk, sour cream, liver), or carotene, which is converted in the organism into the vitamin A (carrot, apricots, peaches, black currant). Fish oil (3 tablespoons per day for adult person, 3 teaspoons — for the child) is prescribed.
Hypovitaminosis PP
In the oral cavity the clinical manifestations of hypovitaminosis PP flow in several stages: the first stage is connected with the appearance of erythema; it is observed already in the prodromal period. Patients complain about the sensation of burning in the area of mucosa of lips, cheeks and especially the tongue. Oral mucosa becomes hyperemized, the tongue is swollen, and filamentary papillae are atrophied. The general state: weakness, headache, insomnia, loss of appetite appear. The pain in the mouth, like neuralgic, appears in stage II. Inflammatory process extends to entire oral mucosa. The tongue becomes clear red and edematic, with a raspberry-coloured tint, resembling the colour of cardinal’s mantle — “cardinal” tongue; the surface layers of the epithelium desquamate, thus the tongue becomes bright, smooth, specular. Sometimes cracks appear on it — “chess tongue”. At this stage the general state of the patient worsens, diarrhea, dermatitis, depression, dystrophia appear. At the stage III the general state of patient is severe. In the oral cavity with the appearance of fuzospirill symbiosis the ulcerous stomatitis develops.
Treatment is specific: saturation of the organism by nicotinic acid (daily dose of 150 mg), and at the 3rd stage dose increases to 300 mg, vitamins of group B: thiamine (20-50mg), riboflavin (10-20mg), pyridoxine (50mg) are prescribed.
Hypovitaminosis J5i
A deficiency of vitamin (thiamine) causes the disease, known as beri-ben- Changes in the oral cavity are not always sufficiently characteristic. The lack of tbi
amine is sometimes accompanied by the neuralgia of trigeminal nerve, increased by painful sensitivity of oral mucosa. Some patients complain about the pain. Frequently bubble lesions of oral mucosa develop, it is more similar to herpetic stomatitis. Phials are localized on the hard palate and on the tongue.
Treatment is specific: saturation of organism by thiamine. Local treatment is symptomatic.
Hypovitaminosis B2
In the absence or deficiency of riboflavin (vitamin B2) in the food ariboflavino- sis develops. The disease is characterized by the inflammation of the lips (angular cheilitis), glossitis, and conjunctivitis.
Angular cheilitis begins with the reddening in the angles of the mouth, and then the painful cracks appear, which resemble perleche. Lips become red, swollen, cracks and erosions appear on their surface. Simultaneously glossitis develops, which is accompanied by sharp painfulness. Filamentary papillae atrophy, thus clear red hypertrophied mushroom-shaped papillae appear across the back of the tongue. As a result of the atrophy of filamentary papillae the tongue becomes smooth, shiny; because of the decreased salivation it seems dry, with many grooves, increased in size. Besides glossitis, conjunctivitis appears, sometimes iritis, eyelids are inflamed, epiphora, burning in the eyps, yisual acuity decrement are observed.
Treatment consists in saturation of organism by vitamins of group B (Bp B2, B12). Local treatment is symptomatic.
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