جامعة بابل | University of Babylon



General pathology

Tissue repair &wound healing:

Healing is a tissue response to wound, inflammation and necrosis, and it’s consist of variable proportion of two distinct processes (Regeneration & scar formation).

1- Regeneration : replacement of damaged tissue by proliferation of adjacent surviving specialized parenchymal cells, like in healing of superficial skin wound that affect only the skin epidermis, so the tissue can completely reconstituted after injury.

2- Scar formation : replacement of damaged tissue by granulation tissue formation and then mature into fibrous tissue, like in healing of deep wound that affect the dermis, and also in healing of internal organs like in scar formation in the heart at site of myocardial infarction.

The type of process for healing influenced by:

Type of tissue affected.(hepatocytes can regenerate while neurons can not).

Severity and duration of injury. (superficial and small skin wounds heal by regeneration, while deep and sever wounds heal by scar formation).

The cells in the body divide into three types according to proliferation ability:

Labile cells: these cells are in continuous division and death, (surface epithelial cells, and stem cells of the bone marrow).

Stable cells: these cells have low level of replication capacity in normal state, but they can undergo rapid division in response to injury like parenchymal cells of liver and kidney.

Permanent cells: these are specialized non-dividing cells, so they can not replaced by identical cells after injury, like neurons and cardiac muscles).

Role of Extacellular Matrix (ECM), in healing process:

provides scaffolding for tissue renewal.

Provide mechanical support for the cells.

Determine cell orientation (polarity of the tissue).

Regulate cell growth and differentiation.

Fibrosis: indicates repair by connective tissue. Its involves the following steps:

Angiogenesis, (formation of new blood vessels).

Migration and proliferation of fibroblasts.

Deposition of extacerlualr matrix.

Maturation and remodeling of the tissue.

Orderly phenomenon of wound healing involving the following processes:

1- Induction of an acute inflammatory process by the initial injury

2- Regeneration of parenchymal cells

3- Migration and proliferation of both parenchymal and connective tissue cells

4- Synthesis of extracellular matrix ( ECM )proteins

5- Remodeling of connective tissue and parenchymal components

Collagenizaton and acquisition of wound strength.

Types of wound healing in the skin:

1- Healing by First Intention (primary union )

The least complicated example of wound repair is the healing of a clean, uninfected surgical incision approximated by surgical sutures, such healing is referred to as primary union or healing by first intention. The incision causes death of a limited number of both epithelial and connective tissue cells. The narrow incisional space immediately fills with clotted blood containing fibrin and blood cells; dehydration of the surface clot forms the well-known scab that covers the wound.

Within 24 hours, neutrophils appear at the margins of the incision, moving toward the fibrin clot. The epidermis at its cut edges thickens as a result of mitotic activity of basal cells, and spurs of epithelial cells from the edges both migrate and grow along the cut margins of the dermis. They fuse in the midline beneath the surface scab, thus producing a continuous but thin epithelial layer.

By day 5, the incisional space is filled with granulation tissue. Collagen fibrils become more abundant and begin to bridge the incision.

During the second week, there is continued accumulation of collagen and proliferation of fibroblasts, while the leukocytic infiltrate, edema, and vascularity have largely disappeared.

By the end of the first month, the scar comprises a cellular connective tissue devoid of inflammatory infiltrate, covered now by intact epidermis.

Note :- Although most skin lesions heal efficiently, the end product may not be functionally perfect. Epidermal appendages do not regenerate, and there remains a dense connective tissue scar in place of the mechanically efficient meshwork of collagen in the unwounded dermis.

2- Healing by Second Intention (Wounds With Separated Edges(.

This type of wound healing seen in case of extensive loss of cells and tissue, as occurs in inflammatory ulceration, abscess formation, and surface wounds that create large defects, the reparative process is more complicated. The common denominator in all these situations is a large tissue defect that must be filled. Regeneration of parenchymal cells cannot completely reconstitute the original architecture. Abundant granulation tissue grows in from the margin to complete the repair. This form of healing is referred to as secondary union or healing by second intention.

Secondary healing differs from primary healing in several respects:

1- Inevitably, large tissue defects initially have more fibrin and more necrotic debris and exudate that must be removed, so the inflammatory reaction is more intense.

2- Much larger amounts of granulation tissue are formed.

3- the phenomenon of wound contraction, which occurs in large surface wounds.

Note: - Whether a wound heals by primary or secondary intention is determined by the nature of the wound, rather than by the healing process itself.

Wound Strength

When sutures are removed, usually at the end of the first week, wound strength is approximately 10% of the strength of unwounded skin, but it increases rapidly over the next 4 weeks. This rate of increase then slows at approximately the third month after the original incision and then reaches a plateau at about 70 to 80% of the tensile strength of unwounded skin, which may persist for life. The recovery of tensile strength results from increased collagen synthesis exceeding collagen degradation during the first 2 months and by replacement of collagen type III by collagen type I, which is the main type of interstitial collagen of the skin.

Factors That Influence Wound Healing

A- Systemic factors include the following:

1- Nutrition has profound effects on wound healing. Protein deficiency, for example, and particularly vitamin C deficiency inhibit collagen synthesis and retard healing.

2- Metabolic status can change wound healing. Diabetes mellitus, for example, is associated with delayed healing.

3- Circulatory status can regulate wound healing. Inadequate blood supply usually caused by arteriosclerosis or venous abnormalities that retard venous drainage also impair healing.

4- Hormones, such as glucocorticoids, have well-documented anti-inflammatory effects that influence various components of inflammation and additionally, these agents inhibit collagen synthesis.

B-Local factors that influence healing include the following:

1-Infection is the single most important cause of delay in healing.

2- Mechanical factors, such as early motion of wounds, can delay healing.

3- Foreign bodies, such as unnecessary sutures or fragments of steel, glass, or even bone, constitute impediments to healing.

4-Size, location, and type of wound influence healing. Wounds in richly vascularized areas, such as the face, heal faster than those in poorly vascularized ones, such as the foot. As we have discussed, small injuries produced intentionally heal faster than larger ones caused by blunt trauma.

Pathologic Aspects of Wound Repair

Complications in wound healing can arise from abnormalities in any of the basic repair processes. These aberrations can be grouped into three general categories:

(1) deficient scar formation.

Inadequate formation of granulation tissue or a scar can lead to two types of complications: wound dehiscence and ulceration.

Dehiscence or rupture of a wound is most common after abdominal surgery and is due to increased abdominal pressure. This mechanical stress on the abdominal wound can be generated by vomiting, coughing, or ileus.

Ulceration of wounds can occur because of inadequate vascularization during healing, for example, lower extremity wounds in individuals with atherosclerotic peripheral vascular disease typically ulcerate. Non-healing wounds also form in areas devoid of sensation, these neuropathic ulcers are occasionally seen in patients with diabetic peripheral neuropathy .

(2) excessive formation of the repair components.

Excessive formation of the components of the repair process can also complicate wound healing. The accumulation of excessive amounts of collagen may give rise to a raised tumorous scar known as a keloid, or hypertrophic scar. Keloid formation appears to be an individual predisposition, and for reasons unknown this aberration is somewhat, it is more common in blacks. The mechanisms of keloid formation are still unknown.

(3) formation of contractures.

Contraction in the size of a wound is an important part in the normal healing process. An exaggeration of this process is called a contracture and results in deformities of the wound and the surrounding tissues. Contractures are particularly prone to develop on the palms, the soles, and the anterior aspect of the thorax. Contractures are commonly seen after serious burns and can compromise the movement of joints, to a degree than required plastic surgery to restore function of the parts affected.

Fractures and healing of bone fractures:

[pic]

TYPES OF FRUCTURES:

1. INCOMPLETE FRACTURE: The bone is cracked, but not broken into two pieces. The best-known incomplete fracture is the fast-healing GREENSTICK FRACTURE from an impact to a child's supple long bone.

2. CLOSED (SIMPLE) FRACTURE: The overlying tissues are intact

3. OPEN (COMPLICATED) FRACTURE: The bacteria have a route from the surface to the bone; perhaps the bone is even sticking out the wound.

4. MULTIFRAGMENTED FRACTURE (formerly "comminuted fracture"): The bone is broken into several pieces.

5. COMPLEX FRACTURE: A curious term for a fracture in which the ends of the bone fragments have done serious damage to the surrounding tissue.

6. PATHOLOGIC FRACTURE: Due to intrinsic disease of the bone; the force would not have broken a normal bone. Seen in osteoporosis, cancer, osteogenesis imperfecta, others.

SEGUENCE OF FRUCTURE NORMAL HEALING PROCESS

1. fracture tearing of blood vessels in medullary cavity, cortex, periosteum.

2. hematoma forms at site of fracture and periosteum is also stripped away from bone surface

3. migration of neutrophils and macrophages into fracture hematoma , these cells phagocytose the hematoma and necrotic debris

4. in growth of capillaries and fibroblasts from surrounding tissue - granulation tissue

5. new osteoprogenitor cells develop from mesechymal precursor cells

6. osteoblasts form

7. osteoblasts migrate into granulation tissue and begin synthesis osteoid .

8. osteoid is lay in haphazard way producing a woven bone pattern

external callus: bridges fracture site outside bone

internal callus: bridges fracture in medullary cavity (and occasionally contains cartilage)

9. once bone ends are closely apposed, ossification between fracture ends occurs

10. by 3rd week, callus is well established but is woven bone (therefore mechanically weak)

11. remodeling of callus takes place over next few months by means of osteoclastic erosion and organized osteoblastic osteoid synthesis, replacing the woven bone with compact organized lamellar bone

for proper fracture healing to take place it is essential that the:

• fractured bone ends be in close apposition

• fracture is immobilized

• patient's healing capacity is adequate.

factors that are Affect normal fracture healing process are:

1. poor blood supply to affected area (e.g. bones such as scaphoid and neck of femur can be associated with avascular necrosis of fracture ragments)

2. poor general nutritional status (particularly where there is protein malnutrition or vitamin deficiencies)

3. poor apposition of fractured bone ends (e.g. wide displacement, entrapped viable soft tissue between bone ends, excessive mobility)

4. presence of foreign bodies (e.g. necrotic bone tissue)

5. presence of infection (particularly for open fractures)

6. corticosteroid therapy

note: when fracture bone ends are not closely apposed, ossification of callus does not occur and the two bone ends are joined by fibrous tissue (fibrous ankylosing) which is unstable

TIME FRAME OF NORMAL FRACTURE HEALING:

• 12 hours: bleeding tops, clot in fractures site

• day 1: local acute inflammation

• day 2: early granulation tissue formation

• day 5: earliest osteogenesis

• 3 weeks: fibrous union and patchy callus

• 6 weeks: continuity of external callus

• 4 months: remodeling completed

COMPLICATOINS OF FRUCTURES:

• delayed union

• mal-union

• fibrous union

• non-union

• soft tissue injury

• infection

• embolism (fatty marrow, air)

• thrombosis

• pseudarthrosis

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Lec.8

Dr. Ali Zeki

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