• Fibroblasts may differentiate into: Bone, Cartilage, Fat Cells & Smooth Muscle Cells

• Cartilage is Type II collagen and ALL the others are Type I collagen

• Fibroblasts are the least specialized cells in the body & are mesodermally derived (classified by

morphology, staining & function)

• The extracellular matrix is secreted by the Fibroblasts & contains Collagen (type I & II), Proteoglycans,

Elastin & Fibronectin.


• Collagen holds the body together & 25% of mammalian protein is collagen.

• It is found in bone, cartilage, skin, teeth, blood vessels & tendons


• It occurs in 2 stages; the first is Intracellular (amino acids ( Procollagen)

the second is Extracellular (Procollagen ( Mature Collagen)

A. Intracellular steps:

( 4 substeps: Polypeptide synthesis, Hydroxylation & Glycosylation, Triple Helix formed,

and finally secretion.

1. Polypeptide Synthesis:

- Within Fibroblast mRNA transcription/translation in the ER (17 possible genetic forms)

- 1000 amino acid residues with terminal extensions

- Sequence is GLY-X-Y where X & Y are any other Amino acid (GLY found 333 times)

- Proline most often in X position (100 times)

- Hydroxyproline most often in the Y position (100 times) [Hydroxylysine often in Y also]

Both may be also found in the X position.

( Glycine is smallest A.A. & allows for helical nature of structure whereas Proline &

Hydroxyproline give structure its rigidity.

2. Hydroxylation & Glycosylation:

- Proline & Lysine must be hydroxlated after they are on chain in the following manner:

- Lysyl hydroxylase acts on Lysine in either X or Y position

- Prolyl-4-hydroxylase acts on Proline in the Y position

- Prolyl-3-hydroxylase acts on Proline in the X position

(remember 3 before 4 ( X before Y so 3 goes with X & 4 goes with Y)

• Hydroxylation is only possible if the following compounds are around:

- Ferrous Ion on enzyme

- Molecular oxygen

- Ascorbic acid (keeps Ferrous ion happy)

- Alpha ketogluterate (substrate)

3. Triple Helix Formation:

- Carboxylation with Glucose & Galactose leads to 3 Alpha chains twisting to form

Procollagen via Hydrogen bonds.

4. Secretion:

- Then Procollagen leaves fibroblast & goes into ECM.




b. Extracellular steps:

( 3 substeps: Hydrolysis of polypeptide bonds, Cross linking & finally Quarter Stagger


1. Hydrolysis of Polypeptide bonds:

- Procollagen Peptidase cleaves the terminal extensions thereby creating “Tropocollagen”

2. Cross Linking:

- The immature collagen is cross linked via inter/intra hydrogen bonds & ( tensile

strength is obtained

3. Quarter Stagger Array:

- The collagen molecules line up in a special array to increase their strength even more & allow for mineralization to occur.


• Some symptoms that may be seen with this disorder are:

- bleeding gums - weak bones - loose skin - lax joints

- Bruising, strokes & aneurysms (due to vascular fragility)

- damaged joints due to loss of cartilage

( This disorder is systemic in nature & affects all type I collagen

( The only way that all type I can be affected is per the 3 conditions:

- genetic (hereditary) - Endocrine - Metabolic (nutrient/vitamins)


|Scurvy |• Hydroxylation step interrupted |

| |( bleeding gums, bruising, weak bones |

|Ehlers-Danlos (humans) & Dermatospraxis (cows) |• Problem with procollagen peptidase (failure to cleave) |

| |( Humans: stretched skin, weak stature, teeth problems |

| |( Cows: bad skin, early death due to infection |

|Marfan’s Syndrome & Osteogenesis Imperfecta |• Hereditary affecting intracellular events |

| |• 4 types of each disease are known |

| |• One osteogenesis Imp. due to mRNA problem |

| |• One Marfan’s is due to failure to form cross links extra |

| |cellularly |



• 5 functions of bone are: - protection (vital organs & brain) - hematopoiesis

- support - mineral storage

- mechanical basis for movement


• Bone is a dynamic constantly changing tissue

• Type I Collagen (organic composition) that provides ((TENSILE STRENGTH ((

• Solid (inorganic particles; ie calcium) that provides ((COMPRESSIVE STRENGTH((

• Organic to Inorganic ratios of bone:


|Child |1:1 pliable, bend then break |

|Adults |1:4 not as pliable |

|Elderly |1:7 quite brittle |


• Although bone is a rigid Tissue; it adapts to stresses (ie Wolffe’s law). Moreover, every 7 years our skeleton is completely turned over.


• Bone is formed from mesenchyme in two ways:

1. Membranous bone that transitions directly from mesenchyme to bone (ie: clavicles, skull bone). It grows by accretion; adding bone to the surface & edges of the bone.

2. Endochondral bone that forms cartilage first & then ossifies forms MOST bones in the body.

- Bony cartilage has chondrocytes that enlarge & leave holes in the cartilage to then have minerals deposit.

- This is followed by 1(, 2( ossification centres, growth plates close & blood vessels


( Carpals & tarsal bones only have 1( site of ossification whereas Vertebral & long bones have 1(, 2( & 3( sites of ossification.

( Females reach skeletal maturity 3 years prior to males around age 15-16.

(( Increased osteoblastic activity is noticed by an elevated Alkaline Phosphatase enzyme & could indicate a rapid bone growth that could be pathological (ie: osteosarcoma, fracture repair, metabolic/endocrine problem) or simply children’s growth spurt.

• Bone is the only tissue in the body that replaces itself when injured. This is unlike skin & Blood vessels that form scars.

• If there is disruption of the growth plate in children, the bone stops growing & we may see a short limb. A disruption of the growth plate is caused by:

- possible fracture or trauma to growth plate

- shearing/compressive loads (compressive loads worst for Growth plate)

- metabolic problem (ie: rickets)

- genetic problem

- hormonal (pre growth plate closure = Gigantism)

(post growth plate closure = Acromegaly)

- bone infection

• Bone matrix is laid down by osteoblasts & appositional Bone growth occurs by:




• Poliomyelitis frequently affects the lower limbs with a predilection to the left one. Its etiology is unknown.

• There are two methods to prevent leg length discrepancies:

- remove the growth plate (of non affected leg). Done in older children around 13-15 yrs. old.

- put pressure on the growth plate by stapling the epiphysis to diaphysis (of non affected leg). Done on children 4-8 yrs of age.


• Bone deposits on the side of compressive force & it erodes on the opposite side where there is no compressive force applied. This is due to the pezioelectric effect.

• Normal bone will turnover & osteoclasts will bore tunnels in the bone to then have ossification occur towards the centre of these passages. Laying down of bone occurs in a lamellar fashion.


• Must have appropriate calcium & other metabolites in blood & bone

• A “load”, “pressure” (specifically LONGITUDINAL)on the bone. Prolonged bed rest (2 weeks)raises the level of Calcium in Urine. Must have at least 3 hours of standing per day to return Calcium levels to optimum levels.

• Gravity is essential to ensure proper mineralization of the bones.

• A viable blood supply to provide oxygen for the cells.



• Fracture means a break, a discontinuity of bone or break in the bone cortex. (in our ABC’s we think of Alignment)

• An old term “broken cortex” could refer to any organ in the body that had a cortex (ie: adrenal or kidney)

( A FRACTURE is the MOST common lesion to a bone!!! & is considered PATHOLOGICAL

( A fracture occurs generally due to trauma; enough to overcome the compressive or tensile strength of the bone.

( We are predisposed to fractures for the following reasons:

- Decreased mineralization (metabolic) - Bone infection

- Decreased blood supply - Collagen synthesis disorder (genetic)

- Life style (sedentary) - Neoplasia

- ( estrogen/testosterone (hormonal)

(( All fractures are pathologies but not all fractures are pathological. (only those that are due to underlying pathologies may be considered as “pathological fractures”)


• Open (Compound): This fracture has bone that is broken & sticking through the skin.

• Closed (Simple): This fracture is not through the skin.

• Partial: ( bone is still somewhat attached

• Complete: ( bone is separated

• Transverse fracture:

• Oblique fracture:

• Green stick fracture:

• Spiral fracture:

• Comminuted (Splintered/crushed): This may occur to flat or long bones

• Compression fracture: Almost exclusively affects vertebral bodies & is due to axial compression. On radiographs looks light area of increased radiodensity. More typically the body will look wedged shaped being more compressed anteriorly. Occasionally the vertebra is collapsed completely.

• Avulsion fracture: This is the forcible ripping or tearing of a portion of the bone (ie: tubercle) by muscles that are attached to it. An example of this is a “Clay shovellers fracture/Coal miners fracture” of C6-C7 spinous process. Now we see this most often in auto accidents.

• Fatigue fracture: These are AKA “Stress fractures” and are due to repetitive low force stress. They may not show up on Xrays & occur primarily in healthy bone. Marching (military) often induces such fractures especially of the metatarsals, tibia & may occur bilaterally. These are easy to correct by simply having the Patient avoid doing the activity which is causing the fracture in the first place.


2) TYPES OF FRACTURES (Continued):

• Collie’s fracture: This is a complete fracture of the distal radius with posterior displacement of the fragment. It is commonly seen in elderly patients & osteoporotic people. It is often caused by Falling on outstretched hands.

• Chance fracture: This is a horizontal fracture through the vertebral body & posterior arch. It generally occurs due to shearing forces applied from the anterior or posterior of the body. This could occur from a head on collision wearing only a lap belt (but lap belt above lap around the abdomen area).

• Jefferson’s fracture: Also called “burst fracture or “Jefferson burst” It involves a complete fracture of the anterior & posterior arch of the Atlas (C1). A common way of doing this is by falling on head or diving into a pool with little water or doing a roll over with a car.

• Hangman’s fracture: This is a bipedicular fracture of C2 & commonly occurs by hanging (need both an extension & rotation component at the neck to occur). Often this occurs in whiplash accidents with person turning their head sideways.


• 3 stages are seen in fracture repairs:

- Inflammation phase (10%) - Reparative phase (40%) - Remodeling phase (70%)

There is an overlap between the phases & time frame affected by health & age of individual.

• The following factors affect the fracture repair:

- nutrition - age - severity of fracture - alignment of fracture

- location of fracture - appropriate level of activity

- immobilization to keep bones aligned preventing further damage & neovascularization occurs


• Occurs from onset of fracture to about 10 days. Overlaps with Phase 2 (reparative phase)

• There is rupture of blood vessels in bone & soft tissue with hematoma filling the gap & seals of the fracture site.

• Tearing of periosteum occurs within first few days & we have bone & soft tissue necrosis

• Around 2-5 days we have fibrin mesh formation & pain is greater due to ( activity of nociceptors & periosteum continues to lift. There is a general deep achy sensation.

• Fibroblasts come in & change into CHONDROCYTES due to lack of blood supply. They start laying down cartilage. The bone ends recede a bit as old bone is removed (we can see a fracture

better after a few days).

• Macrophage & necrosis continue.

• Around the 5-10th days we begin to see a soft tissue Callus being formed (Procallus) by chondrocytes & soft tissues. Macrophage activity ongoing.




• Occurs around 1 week to a few months time. Early part overlaps with Inflammatory phase.

• Osteoclasts & mononuclear cells clean up area & neovascularization occurs. Fracture may appear wider in X rays also.

• A Callus formation is seen as a “Cloud” around the fracture area. Osteoblastic activity goes way up (we have ( in Alkaline phosphatase activity)


• This phase overlaps with Phase 2 & occurs around one month after fracture occurred. Generally occurs once the callus has sealed off the bone.

• Bone begins to adjust strength & shape following Wolffe’s law & there is still a high level of Osteoblastic activity going on.


( Alkaline phosphatase is released in greater amounts when Osteoblasts are laying down bone especially when we having the following conditions:

- Bone repair (many fractures) - Children

- Cancer’s (bone building tumours such as osteosarcoma) - Infection

( Erythrocyte Sedimentation rate (ESR) is the rate at which red blood cells are setting. It occurs in a higher rate especially when inflammation is present. There is no such thing as a “Neg” ESR.

We may see a high ESR in the following conditions:

- Inflammation stage of fractures - Infection (bone)

- Rheumatoid arthritis - Malignant neoplasia

( Radio nuclide imaging such as bone scans may be set to visualize specific areas of ( osteoblastic activity. The radioactive nuclide is excreted via the bladder & high levels may be noted in the bladder (not necessarily an indication of pathology there).

Although very sensitive (can detect as little as 4% bone activity) it is not specific & further tests need to be done to determine what is seen on the bone scan (ie: is the area neoplastic, infection, etc)



General info:

• Calcium is involved in many reactions some of which are:

- Enzymatic reactions - Mediates hormone secretion & events - Neurotransmitter

- Muscle contraction - Blood clotting - Cation in bone & teeth

• Normal physiological limits for Calcium in blood are between 8.6 - 10.6 mg/dl. This does not vary more than 10% from set point in a given 24 hour period.

• In the body only 50% of calcium is biologically active (available). 40% is protein bound & 10% is in non ionic form such as calcium bicarbonate.

Calcium Turnover:

• Essentially, we turnover calcium in our body on a daily basis. In a 1000 mg diet of Calcium the following happens:

- 350 mg absorbed into ECF via Gut & simultaneously 150 mg secreted into gut

- 800 mg secreted into feces & about 200 mg secreted into urine

- At the bone level we have about 500 mg being secreted & absorbed simultaneously via the Rapidly exchangeable pool.

( Take home message is that the Gut, Bone & Kidneys do the CALCIUM REGULATION

• Calcium absorption is inversely related to Gastrointestinal intake. Therefore, take in a high quantity of Calcium in diet & a smaller percentage will be absorbed.


General Info:

• Phosphate is found and used in the following areas:

- Glycolytic compounds - ATP,ADP, AMP, Creatine phosphate - Major Bone anion

- Cofactors (NAD & NADPH) - Lipids such as phosphotidyl choline

- Covalent enzyme modifiers

• The normal physiological range of Phosphate in blood plasma is 2.5 - 4.5 mg/dl. Unlike Calcium the amount of Phosphate absorbed from the diet is constant.

( Major mechanism in Phosphate balance is Urinary excretion.

Phosphate turnover:

• Essentially, if we have an intake of 900 mg of Phosphate, the turnover is as follows:

- 300 mg from gut go into feces & 600 mg form gut go into ECF

- From the ECF 600 mg are excreted via the kidneys & into the urine

- We have a simultaneous turnover between the bone & Rapid exchange pool of 250 mg.



• The parathyroid glands are the MAJOR regulators of Plasma Calcium

( Calcium drives the System! PTH secretion is inversely proportional to plasma Calcium levels & PTH is released within minutes to re-establish equilibrium

• Hypocalcemia occurs when the calcium plasma level drops below 8.6mg/dl (if hypocalcemia lasts for a long time, then gland hypertrophy occurs)

• Hypercalcemia occurs when the calcium plasma level rises above 10.6 mg/dl (if hypercalcemia lasts a long time, then PTH synthesis & stores are shut down.

Role of PTH:

• Phosphate acts indirectly on PTH through a physiological mechanism that lowers the Ca++ levels. An injection of Phosphate would have Ca++ drop & then PTH would increase. Then the PTH would have

kidneys dump the extra phosphate via the kidneys to prevent hyperphosphatemia.

PTH Action on Bone:

• PTH stimulates osteolysis putting Ca++ back into plasma. However, to do this it must stimulate osteoclasts which begin the resorption of bone & ( many bone constituents are liberated. PTH also shuts down

osteoblasts & inhibits collagen synthesis (VitD)

PTH Action on Kidneys:

• PTH will cause Ca++ to be reabsorbed from distal tubules but MOST IMPORTANTLY IT PREVENTS PHOSPHATE REABSORPTION

• It also stimulates synthesis of Vit D metabolite

PTH Action on GUT:

• It stimulates 1-25 dihydroxy OH2-D3 indirectly ( ( Ca++ across lumen

• We believe there are PTH receptor cells in the lumen??


( The most common cause is a single parathyroid adenoma

( Signs & symptoms are similar to Hypercalcemia which include, dull mentation, lethargy, muscle weakness & hypoflexia, anorexia & constipation. The hypoflexia occurs because there is so much Ca++ that the Ca++ gates are down regulated

( You will see Renal stones, & with persistent hypercalcemia there may be reduced renal function with possible irreversible renal failure.

( Peptic ulcers are a sequela

Long Term Effects of PTH Secretion on Bone:

• Bone is resorbed irregularly with weakening of bone & pain because periosteum becomes irritated. Fractures occur because of pathology & deformities are common.

( Areas where there is focal bone resorption are called “Brown Tumours” due to many micro fractures and small hemorrhages.

( Another common condition is called “Osteitis Fibrosis Cystica” where the area fills with fibrous tissue.

( Both conditions revert back to normal when the hyperparathyroidism is reversed.



Types of Hyperparathyroidism:

• There is a Primary Hyperparathyroidism which is quite common. The problem is confined to the Thyroid gland. It no longer responds to rising levels of Ca++ & is due to a single parathyroid adenoma.

• Secondary Hyperparathyroidism is due most frequently to chronic renal failure or malabsorption of Ca++. In this case the PTH is released but Ca++ levels stay the same. The gland becomes hypertrophied & the Ca++ plasma levels are low to normal with very low Phosphate levels if Kidneys are healthy.


General Info:

• Signs & symptoms are those of Hypocalcemia such as

- Hyperactive reflexes - Spontaneous muscle contractions - Convulsions

- Laryngeal spasm with airway obstruction

• There is insufficient PTH to rid kidneys of Phosphate & Calcium levels are low. Often this is due to inadvertent surgical removal of the gland.

• The most common cause is autoimmune idiopathic atrophy & rarely is it end organ resistance to receiving PTH. Often seen with a diminished Ca++ & very little Vit D metabolite present. Bone resorption decreases.

( If we were to administer exogenous PTH to a patient with damaged parathyroid glands; the Ca++ would go up & the Phosphate levels would decrease (we would expect this to happen)

( A patient with unresponsive target tissue that was administered a dose of exogenous PTH would not see a change in the Ca++ or Phosphate levels because the end organs are damaged.

( Treatment of Hypoparathyroidism is by administration of Vit D ( 1-25-OH2D-3) & Calcium to make up for the drop in PTH.


General Info:

• Calcitonin is the physiological antagonist to PTH hormone (PTH raises CA++ levels whereas Calcitonin decreases PTH levels). It is produced by the parafollicular cells of the thyroid gland.

Actions & Effects of Calcitonin:

• Through various membrane receptors & cAMP calcitonin helps in sequestrating Ca++ into the mitochondria, ( lowering the Ca++ plasma levels.

• Ca++ plasma levels fall off rapidly (moreso in kids than adults) & osteolysis/bone resorption is inhibited.

• Although Calcitonin has the same effects on Phosphate as PTH does the mechanism is different. It is believed that Calcitonin enhances Ca++ & Phosphate uptake by the bone.



General Info:

• Two sources of Vitamin D are D3 (produced by skin exposure to UV) & D2 from plant steroids

• Vitamin D may act as a bone builder or bone breaker. We know for sure that the 1,25 metabolite is a bone breaker. The 1,25 metabolite works synergistically with PTH to break down bone (PTH also causes more 1,25 to be produced during the breakdown of the 25OHD3 in the Kidney).

• We believe that Vitamin D3, 25-OHD3 & 24,25OH2D3 metabolite are bone builder in nature.

Action of 1-25 metabolite:

• In the kidney it stimulates production of Calbindin. Calbindin helps in Ca++ & Phosphate absorption from the gut. In the bone it ( osteoclast activity & ( osteoblast activity.

Action of Vitamin D:

• Bone building & mineralization is dependent on Vitamin D. Muscles store Vitamin D & patients with muscle weakness have Vitamin D deficiency.

Vitamin D Toxicity:

• Overdosing & abnormal sensitivity to Vit.D may lead to toxicity.

( We see increased plasma & urinary levels of Ca++ & this shuts off PTH secretion . The symptoms are those of Hypercalcemia & differential diagnosis of the two reveals the following:

|Blood test |Hyperparathyroid patient |Vitamin D toxicity |

|Plasma Ca++ levels |( levels |( levels |

|Plasma PTH levels |( levels |( levels |

|Plasma Phosphate levels |( levels |normal to slightly elevated |

( Treatment is by reduction of Vitamin D or administering Calcitonin/cortisol & allow the Vitamin D to clear out of the system (this may take months)

Vitamin D Deficiency:

• May be due to lack of sun, ( dietary intake, G.I. pathology or problem in Liver/Kidney hydroxylation.

• With a Vit. D deficiency we see a drop of Ca++ in plasma & an increase of PTH with simultaneous loss of

Phosphates in the urine (the kidneys hold on to the Calcium in an attempt to reestablish equilibrium)

• This leads to a reduction in bone mineralization. However, as loads are imposed on the bone, Wolff’s law

feels that there is a greater stress on the bones. So a large quantity of osteoids are formed. However, bone

building can’t occur because of the imbalance between the calcium & phosphate.

( Vitamin D deficiency leads to Osteomalacia (adults & no open growth plates) or Rickets (children with

open growth plates):


|Slightly reduced plasma Ca++ |Slightly reduced plasma Ca++ |

|Greatly reduced Phosphate levels |Greatly reduced Phosphate levels |

|High levels of PTH |High levels of PTH |

|( Treatment is to give Vitamin D & Ca++ |( Treatment is to give Vitamin D & Ca++ |

|( We see that the bone is more organic than inorganic & that there is |( Xrays reveal osteopenic bones with radiodensity changes & little |

|lack of Epiphyseal cartilage mineralization or growth of endplate . |bony deformations |

|( Most often seen btwn 6mths-2yrs age |( Patient has bone pains, muscle weakness & pseudo fractures |

|( Xrays reveal Bones that are bowed with widened growth plates |(seams of demineralization & not real fractures) |

| |( Bone is deformed but does not break & condition reversible if |

| |caught soon enough. |



General info:

• Osteoporosis is a term for a variety of conditions. The bone is healthy but there is a reduction of Bone mass.

( Osteoporosis is the most common cause of pathological fractures & costs $1.5 billion/year

( Mostly elderly affected & may lose independence. Many die 1 year post fracture due to fat emboli.

( We attain our peak bone mass (1:4 ratio) around 30-35 years of age & there is no difference between males or females. Diet & exercise are important in attaining optimum bone mass.

( 1 in 2 females will become osteoporotic & 1 in 40 males

Risk & Contributing factors affecting Bone Loss:

• Caucasian, small frame, thin individual with family history of osteoporosis

• Drugs such as steroids, heparin that leach bones, Phosphate & cancer treatments

Clinical diagnosis & treatment:

( ESR, Calcium & phosphate levels & Alkaline Phosphatase all within normal limits

( Treatment consists of exercise, diet & Fall prevention for the elderly

( Further treatment consist of a variety of drugs such as Calcitonin, Hormone replacement & Fosamax



• Acromegaly is a rare disorder that affects 3 in one million births & is more common in females by a ratio of 3:2. It is a

Growth Hormone abnormality of skeletally mature individuals due to a pituitary tumour in early adult life (20’s).

( We see large metacarpals with wide thick hands.

( The jaw is enlarged & the frontal bone shows evidence of “Bossing”. Moreover the bottom teeth are more anterior

than the upper teeth.

( On the feet we see an excessive amount of tissue at the heel pad (greater than 20 mm)

( The joints are ultimately affected & DJD ensues.

( Treatment is removal of affected portion of pituitary gland, radiation therapy & somatostatin (antagonist to Growth Hormone)



• It is a thickening & disturbance of the normal architecture of the bone due to a problem with excessive resorption &

remodelling of bones (bones take on a mosaic appearance)

• It used to be called “Osteitis Deformans” because it was believed that there was an inflammation of the bone, causing it

to deform (however, we don’t know what the etiology is) [NBCE choose Virus]

• It occurs between 5-11% of population over 60 yrs & affects males more often. It seems to have a particular affinity

for Northern European descent.

(( The bone size gives the disease away as very few other diseases cause bone to increase in size

( May be monostotic or polyostotic & affects pelvis, skull, spine & tibia


• There are 3 stages in Page’s disease.

a) Stage 1 - Osteolytic: high rate of osteoclastic activity reducing bone density

b) Stage 2 - Mixed Lytic/Blastic: osteoclasts/osteoblasts are active at same time

c) Stage 3 - Sclerotic (burnout): Bone growth returns to normal & radiodensity ( & bones are larger than before

• The process occurs over years (20-30) and it is possible that it starts up again after it has stopped.


( Patients are asymptomatic (95%) of the time

( Telltale signs are enlarged hat size, Sabre shin, Pathological fractures (due to abnormal pattern of remodelling)

( A condition known as “Paget Steal” occurs with reduction of Blood in circulation because much of it is stolen &

hidden in the enlarged bone. This leads to Heart failure because heart has to work harder & cardiomegaly ensues.

( Platybasia may occur which is a softening of the skull at its base. Skull sinks down & sits on C1 affecting Cervical

nerves. Cranial nerves are affected by narrowing of the foramen in which they pass in the skull.

( Rarely (1-10% of time) do we see malignant degeneration occuring only with polyostotic disease.

( The Alkaline Phosphatase will be normal & so will the ESR. Only a Bone scan will reveal areas of activity.


( Keep an eye on the patient’s circulatory system & in polyostotic disease check for malignancy

( There is one Medication “Fosamax” which may be helpful but it has side effects. It is also cumbersome to use because must be taken at 6 in the morning & then patient must stay upright for 1/2 hour.



• The name implies lack of cartilage at the growth plate of the bones & it is the most common form of

Dwarfism (ALSO MOST COMMON GROWTH PLATE DISORDER NBCE)resulting in 1/40,000 births.

( The Achondroplastic patient present with a normal axial skeleton but a shortened appendicular skeleton.

Their arms & legs are shorter than normal. The bones are thicker at muscle attachment areas & become wavy in appearance.

( Intellectually they are normal & have a normal life span


• A syndrome is a complex of symptoms that involves 1 or more body systems

• Marfan’s syndrome is a disorder of collagen synthesis involving the following areas of the body:

- skeleton - Lens of eye - Mitral valve prolapse (1in 10)

- Vascular system (fatal aneurysms of aortic arch & descending aorta)

( The syndrome occurs in 1/10,000 births & patient has long slender extremities with Arachnodactyly & extreme ligamentous laxity (double jointed)

( Patient is long, slender & often athletic (basketball player)

(( Life expectancy (40 yrs) is shorter & must monitor vascular system

( Bones are described as thin & gracile

( There is no contraindication to adjusting


• This is imperfect bone formation & is AKA “brittle bone disease”. There are 4 types of which Type I is least severe & Type II is most severe.

• Disease is due to a defect in collagen synthesis & therefore affects blood vessels, teeth, tendons/ligaments, eye lenses & joints.

( Type I is called tardia & has decreased bone density, fractures & bowing deformities. The sclera of the eyes appear blue because they are thin. Hearing loss occurs du to bony deformities. teeth are small,

yellowish & blue.

( Type II is called congenita & is a fatal condition. Bones are so brittle that newborns break bones simply

through breathing process.


• AKA Marble Bone Disease or Albers Schonberg disease [NBCE] because the bones appear radiodense.

• A mild case is autosomal dominant & leads to normal life whereas a lethal case is autosomal recessive & lethal.

( In this disease the osteoclasts are hypofunctioning & remodelling doesn’t occur as it should ( there will be areas of ( radiodensity & the medullary cavity will be missing.

( Although there is a lot of bone it is brittle in nature & prone to pathological breaking.

( Patients have a shorter lifespan due to ( hematopoeisis, ( RBC/WBC. PTH is normal to slightly elevated.

( Patient may be adjusted depending on the extent of the disease.



• This is an infection of the bone marrow & is usually insignificant.

• The organism gets into the bone by one of the three following mechanisms:

- Hematogenous (vascular supply) - Implantation (cut & scrape of bone)

- Direct Extension (muscle tissue or other tissue direct to bone)

A. Acute Pyogenic Osteomyelitis:

• This occurs usually because of a bacteria (S. aureus 90%) & spreads Hematogenously. Often due to disrupted blood vessels from trauma.

( Most often seen in metaphyseal area of bone. Children below 15 yrs. most often affected because immune system is not fully functional.

( There is rapid & high fever with severe throbbing at sight of infection with possible pathological fracture.

(( Extremely aggressive & must act quickly because bone can be destroyed in 24 hours. However, 10% of cases become chronic in nature & may last for 20-30 yrs. Complications

include pathological fracture, draining sinus (pus drains through skin), Squamous cell carcinoma

& potentially osteosarcoma.


• Commonly called Pott’s disease [NBCE]. 1-3% of patients with Pulmonary TB develop Bone tuberculosis. This is most often seen in prisons & immunosuppressed individuals.

• The condition is difficult to treat & attacks bones with high oxygen content. Therefore look for it in the spine (especially vertebral body). Travelis via direct extension.

( Complications include pathological fractures, neurological involvement (due to IVF compression), arthritis & abscess (may drain through medial thigh)

( Bone looks porous in X ray views. Patients develop “gibous deformity” aka hyperlordosis.


• This is a chronic bone infection & may be congenital or Acquired.

a) Congenital:

• Changes are seen as early as 5 months in utero & epiphyseal growth plates are destroyed & become wide. Cortex thickens (reactive bone formation). Therefore child has short limbs.

b) Acquired:

• This is acquired through STD.

• Syphilis loves the skull & anterior tibia (Sabre shin due to layering of bone)

( Symptoms appear 2-5 years post infection . In the skull we have lysis & collapse of nasal bones

& palate (often perforated)

( Treatment is very difficult



• Cysts are areas of contained fluid (mostly protein) accumulation lined with fibrous tissue. Often they occur because of trauma .

• There are 2 types:

a) Unicameral:

• These are one chamber AKA “Simple or Solitary” & occur 3 times more often in males than females & seen in children up to 14 years of age.

( They are NOT NEOPLASMS. They are made up of loose fibrous tissue with osteoclasts, macrophages & reactive bone.

( They are round/oval in shape & they tend to expand the bone & cause bone resorption (they generally do not penetrate out of the bone however). On Xray you will see Eucentric location with decreased radiodensity.

( Look for them in the Humerus & Femur

( Treatment is via excision but tend to reoccur frequently

( Do not confuse with Brodie’s Abscess which is an area of wrapped up infection .

b) Aneurysmal:

• This is NOT a NEOPLASM. It is a cavity filled with blood & blood flows into & out of the cavity.

(It generally leaves the bone intact & doesn’t break through the cortex. It is smooth

externally, but internally appears sponge like with many septa (soap bubble appearance).

• The cellular components include granulation tissue, Giant cells & some trabeculae.

• We don’t know what causes them but suspect trauma or genetic factors.

( Often seen in males/females equally after the age of 20. There will be pain/swelling or sometimes be asymptomatic (only be painful if fractured)

( Treatment is curettage & pack with bone chips to trick body into thinking that the bone is fractured. In areas such as spine Radiation therapy may be useful to starve out

blood supply.



• The following cell lines live in bone:

- bone (osteoid) - cartilage - fibroblasts - blood cells

- blood vessels

(( Neoplastic growths do not cross growth plates (cartilage) because these areas are Avascular. Neoplastic growth requires oxygen to proliferate.

• A primary bone tumour is one that arises from cell lines that are normally found in bone & may be benign or malignant.

• A Secondary bone tumour arises from outside of the bone & ALWAYS is METASTIC DISEASE. The 3 mechanisms responsible that allow this to occur are:

- Hematogenous spread - Direct Extension - Implantation (ie biopsy) not common

(( See Contrast sheet by Russell Erhardt for BENIGN VS MALIGNANT GROWTHS


• There are 3 types:


|Osteoma (benign) |• Benign tumour that is primary in origin. It does not invade the bone. |

| |( We see well formed bony projections & it grows off the surface of bone. |

| |( Commonly seen around the face & skull |

| |( Surgically removed if they bother the patient |

|Osteoid Osteoma (benign) |• Occurs in males more than females & age range is 5-25 yrs [NBCE] |

| |( They are small & generally less than 2 cm in diameter & area is called a NIDUS |

| |( The nidus has tiny trabeculae & vascular growth & on XRAY presents as a |

| |radiolucent area with thick sclerotic border. Found most often near ends of long |

| |bones. |

| |( Patient is young & complains of night pains [NBCE]. These pains are partly due to |

| |the fact that there is ( PGE2 that causes vasodilatation & ( pain sensitivity. (aspirin |

| |( the pain by inhibiting PGE2) |

| |( Unlike other Bone forming tumours this one is painful [NBCE] |

| |( Treatment is surgical excision after maturation of neoplasm (may be months wait for |

| |patient) |

|Osteosarcoma (malignant) |• There are 2 presentations. They are composed of osteoblasts, fibroblasts & chondroblasts. Very few cases |

| |in US. |

|Primary O’sarcoma |• Arise from the bone cell lineages. Found more in males below age 20 in the long bones around the knee. |

| |( Patient presents with pain due to aggressive nature of disease (much necrosis, |

| |periosteum lifts, swelling & deformity with red/hot skin over area involved). |

| |( Radiograpically, difficult to see transition from healthy vs unhealthy bone. |

| |Cortex is disrupted & CODMAN’s TRIANGLE is seen with Starburst |

| |appearance. Adjoining tissue is invaded. |

| |( The bone appears to be moth eaten externally & internally we have much |

| |necrosis. |

| |(( Metastasis to Lungs, Bone & Brain with 90% patients dying from this. |

| |( Treatment is surgery (amputation), then chemotherapy & radiation. Survival rate |

| |is 60%, 5years. |

| |• Arises form pre-existing bone pathology or carcinogenic influence such as |

|Secondary O’sarcoma |infection, paget’s disease, radiation therapy etc. |

| |• Found in males most often over age 25 & look for it in the FLAT bones (pelvis |

| |most often). Only 25% of osteosarcomas are secondary. |



• There are 3 types of this Cartilage based tumour:


|Osteochondroma |• This is the most common benign bone neoplasia [NBCE]& may present in 3 varieties. |

| |Three is bony exostoses with a Cartilage cap & fibrous membrane. |

|Solitary |This is most common type. Only 1% undergo malignant degeneration. May involve 2 or 3 bones & there is no |

| |family history. ALWAYS grow away from joint space. |

| |As above but with more of them |

|Multiple | |

| |• There may be between 6 - 100’s of osteochondromas. Most often occur near end of long bones. There IS |

|HME (hereditary multiple exostoses)|Family history & males 3:1. These are painless lumpy joints. |

| |• Growth plates may be affected as they are left behind & begin forming bone. |

| |• Up to 25% may become malignant & change into chondrosarcoma. |

| |( Treatment is surgical excision |

|Chondroma | • More often in males & generally asymptomatic due to slow growing mature |

| |cartilage. Develop over 10-15 yrs. There are “island of cartilage” left behind. |

| |• Most often occur as solitary lesions that are enclosed by vascular & fibrous |

| |stroma. |

| |( Asymptomatic unless pathological fracture occurs |

| |( Treatment is surgery |

|Chondrosarcoma |• Very rare bone pathology that develops very slowly & only metastasizes late in the process. |

| |( We see malignant chondrocytes, necrosis, cystic changes & hemorrhage. |

| |( Mainly seen in ribs, shoulders & pelvic girdle |

| |( Tissue appears grey-white translucent with cysts/necrosis centrally. XRAYS show |

| |“stippled” calcification & localized bone destruction & expanded bone |

| |( Patient presents with a local mass or fracture |

| |( Surgery is indicated but neoplasia may metastasize to Lung, Liver, Kidney, Brain |

| |with 30-90% 5 year survival rate. |

| |(( Because it is so slow a process chemo & radiation therapy don’t work well! |

| |• May occur as Primary or Secondary chondrosarcoma’s: |

| |75% are of this kind & seen in males about 45 yrs of age. NO ETIOLOGY |

|Primary |25% are of this kind & previous etiology is present (infection, paget’s etc) |

|Secondary | |



• There are 3 types of Fibrous tumours:


|Fibrous Dysplasia |• This is a slowly expanding lesion that lives near the end of long bones (femur, tibia, ribs, face) |

| |• Only about 1% go onto become malignant. The majority are monostotic with some polyostotic |

| |( The contents include fibroblasts, collagen, irregular trabeculae, cystic degeneration & some |

| |hemorrhage. In both cases we see well defined radiolucent lesion with enlarged bone |

| |Monostotic: 75% of patients have these & no age preference. |

| |( The patient is often asymptomatic, bone may be large & first indication is often a |

| |pathological fracture. |

| |Polyostotic: A rarer form involving 1/2 the skeleton. |

| |( The bones are deformed in size & shape with limb length discrepancy often seen. Often |

| |first indication is pathological fracture |

| |( Treatment in both cases is monitoring & possible surgical consult to repair bone |

|Fibrous Cortical Defect |• This is AKA Non Ossifying Fibroma or Fibroxanthoma & is most likely NOT a Neoplasm |

| |• It is very common & occurs in 30-50% of kids over 2 yrs age |

| |( Lesion are between 0.5 to 6 cm in size & often located in tibia, fibula & femur. |

| |( They appear as small area of bony cortex that is replaced by well demarcated soft/pliable |

| |yellow gray tissue that is composed of fibroblasts & giant cells. |

| |( The patient has nocturnal leg pain & occasionally pathological fracture |

| |(( No new bone is formed |

| |( No treatment as they disappear on their own |

|Fibrosarcoma |• It is composed of primitive connective tissue & fibroblasts with sheets of malignant fibrous |

| |tissue. |

| |• It is most often seen in males between 30-40 yrs age & develops slowly |

| |( There is local low grade pain that often refers to joints. Average about 2 years duration |

| |unless pathological fracture occurs first. |

| |( Treatment is surgical removal & if left untreated will metastasize to the lungs & lymph nodes |



|Giant cell tumour |• This is an uncommon tumour with cells of origin being monocytes & macrophages. Cells are large & |

| |multinucleated. They are benign 75% of time |

| |( Preference is in the epiphysis of long bones & primarily as a very large solitary lesion with a SOAP |

| |BUBBLE appearance on radiographs surrounded by a thinning cortex. May also see septa within. |

| |( There are areas of hemorrhage, cystic formation & yellow necrosis |

| |( The patient complains of non specific local pain (due to microfractures) & tenderness. May lead to |

| |Pathological fractures. |

| |( Treatment is surgical removal for malignant ONLY while monitoring the benign ones. For malignant also |

| |use drug therapy & radiation |

|Multiple Myeloma |• This is malignant proliferation of Plasma cells [NBCE] that infiltrate bone making small lesions (1-5 |

| |mm) [NBCE] & radiographically appear lytic. |

| |• Occurs more often in males than females in the age category above 70 yrs age. Often patients are |

| |farmers |

| |that were exposed to pesticides & there is causal link to men’s hair colouring |

| |( Clinically we see anemia due to loss of hematopoeisis & bone deossification. There is renal failure due|

| |to |

| |( production of immunoglobins in 95% of cases |

| |( Patients have pain worse in day time & aggravated by activity due to microfractures. Often pain comes |

| |on after slight exertion very rapidly. Patient begins to lose weight has cachexia & anemia with |

| |unexplained osteoporosis |

| |( It loves to live in vertebral body due to large blood supply (also found in skull & pelvis) |

| |( Radiographically “punched out Lesions” & best seen on Xray than bone scan (due to no osteoblastic |

| |activity). Lesions DO NOT have SCLEROTIC border |

| |( Treatment is palliative as there is no cure. 90% patients die within 3 years. May try radiation, chemo |

| |& |

| |nutrition |

| |( Doesn’t fit the Tumour mold like other tumours |




|Hemangioma |• This is a congenital vascular variant with large thin walled blood vessels & sinuses surrounded by bony|

| |trabeculae & reactive bone. It is Benign. |

| |( It is clinically silent & not prone to pathological fractures. Patient may complain of |

| |localized pain, muscle spasm & neurological compromise |

| |( Radiograpically has Corduroy Cloth appearance [NBCE] with coarse vertical striations |

| |separated by radiolucencies (Unlike osteoporosis, Hemangioma affects ONLY 1 bone ) |

|Ewing’s Sarcoma |• We don’t know what causes this pathology or what it is made out of. It is described as “small round |

| |closely packed malignant cells” [NBCE] |

| |• The tumour is highly necrotic & possibly linked to genetics with a Male VS Female ratio 2:1 & |

| |is seen most frequently around 5 - 30 yrs of age. |

| |( Unlike other tumours this one has a preference for mid shaft of long bones & the pelvis & |

| |originally comes from the medullary cavity expanding outwards. It will cause lifting of the |

| |periosteum & necrosis of medullary cavity & radiographically looks like a piece of bone |

| |missing. We will also see an onion skin appearance of the periosteum. |

| |( Patient presents with pain (worse at night) at midshaft of long bone with swelling, heat, |

| |redness & you will palpate a mass extending 360( around the bone. |

| |( Surgical treatment is indicated with radiation/chemotherapy. There is a 75% 5 yr survival rate |

| |( This is not a bone forming tumour |

| |(( An “Extraosseous Ewing’s Sarcoma” is identical to above but found outside the |

| |skeleton within the organs such as liver/lung etc. IT did NOT metastasize from Bones |

| |(no pathology in the bone). Current theory is that this is some sort of neurological tissue |

| |[NBCE] |



|Secondary Bone tumours |• These tumours arise from other areas in the body & migrate to the bone. This is the most |

| |common malignant tumour of the bone [NBCE] giving rise to 70% of malignant bone |

| |tumours. |

| |• It most often arises from the breast (females 70% of time & affecting upper thoracic & |

| |cervicals), lungs, prostate (males, 60% of time & affecting the lower back/sacrum) & kidneys |

| |• The malignant cell may travel via hematogenous spread, direct extension & implantation to the |

| |bone. |

| |( We see this in second half of life time & rarely in children. The patient presents with |

| |weight loss, anemia & fever in advanced stages. There is skeletal pain at night. |

| |( Radiographically the bone will be seen as “Moth eaten or Permeative” in appearance due |

| |to the osteoblastic/osteoclastic activity going on. Essentially the bone is being replaced by |

| |the invading malignant cells (which may be breast, lung, prostate or kidney cells) |

| |(( You will NOT see periosteal lifting, or soft tissue mass (cortex rarely broken). The |

| |lesions are small (3-5 mm) & bone is not expanded but there are multiple sites of |

| |involvement) |

| |( Diagnostically you would do a bone scan, MRI, Alkaline Phosphatase (which may be (,( or |

| |normal depending on type of bone tumor present) [On exam say (] |

| |(( Prognostically the outcome is not good for the patient. Treatment options are radiation, |

| |chemo (surgery is not an option except for primary site of tumour. For instance in the G.I. |

| |tract where there may be obstruction). |

| |( Chiropractically we can adjust using soft type techniques, activator, SOT m nutrition & |

| |moral support |


NB: NBCE LOVES JOINTS. KNOW THEM BY FUNCTION & STRUCTURE (A Schindylesis synarthoris is between Vomer & Ethmoid bone)


• Bones are bound together across a joint space by Skeletal ligaments that blend with the fibrous capsule. Most of the ligaments run in same direction & are composed of Type I collagen fibres that allow for LITTLE stretch.


• The internal aspect of a joint is lined with a synovial membrane except for the Articular Surface. Because the synovium is arranged in villi/microvilli it covers a large surface (ie: in the knee the membrane covers equivalent of 100 sq. meters). Histologically, the synovium is not a true membrane because it lacks a basement membrane & gap junction. It is composed of 1-5 cell layers thick of A or B cells.

- Type A cells: These are macrophages that contain lysosomal enzymes & clean up debris

- Type B cells: These are secretory & produce Hyaluronic acid

• There is a subsynovial tissue that is very vascular & areolar (CT meshwork). Some joints have the synovium applied to dense CT of joint capsule & in others, like the knee the synovium overlies a fat pad posteriorly.


• It controls diffusion into & out of the joint, ingests debris, & secretes Hyaluronate, immunoglobins & lysosomal enzymes that lubricate the joint (major function).

• Because Hyaluronate is a large negatively charged molecule it attracts water. it ( allows for proper viscosity of the synovial fluid. (Hemophilacs bleed into joints & compete for the Hyaluronic binding sites & change its ability to carry out its function properly).

( There is about 1-4 ml of synovial fluid which is composed of Plasma filtrate & synovium. The synovial fluid does not contain fibrinogen & ( cannot clot. Also doesn’t contain alpha 2 macroglobulin. The fluid should be clear & straw coloured. (cloudy/turbid fluid indicates a problem)


• Its function is to absorb shock & lubricate the joint surface. It should appear smooth white & semirigid & not exceed 6 millimeter in thickness (due to fact that it survives on diffusion alone)

( The Holmdahl/Ingelmark experiment showed that the cartilage size ( with activity & ( with inactivity. This ( in size helped absorb shocks better & help spread the load more evenly on the joint surfaces

( Histologically there are 5 zones of articular cartilage as follows:

- Tangential (farthest from bone) - Transitional - Radial

- Calcified - Subchondral (closest to bone)

( Essentially the radial zone & calcified zone form the “BLUE LINE/TIDE MARK” & is significant for the following reasons:

- interface between mineralized/unmineralized bone

- Divides nutritional source for chondrocytes. (On bone side via epiphyseal blood. On cartilage side via diffusion)

- cartilage side chondrocytes replicate & migrate towards the surface. Bone side the chondrocytes only divide with appropriate stimulus. (IE; In acromegaly we have chondrocyte replication on bone side & DJD is a sequela)

• Chemically the articular cartilage is hyperhydrated tissue (68-78% water by weight). The remainder is Type II collagen, proteoglycans with some lipids, phospholipids & lysosomes. The breakdown of the proetoglycans in DJD/RA leads to loss of cartilage ability to resist wear.

( Cracks may develop in the cartilage which then prevents the rate of synthesis with keeping pace for required repair.


• There are 4 nerve endings in a joint as follows:

- Encapsulated (respond to mechanical stimuli such as pressure)

- GTO’s (respond to tension generated at musculocutaneous junction

- Pacinian corpuscles (respond to acceleration/deceleration of joint movement

- Free nerve Endings (Pain receptors)


• This is closed flattened CT sac that contains small amount of fluid.

• Deep bursae develop before birth. More superficial ones develop due to friction (ie: around joints, tendons etc)


• These are similar to bursae but they envelope the tendons. Mesotendons are gaps in the sheaths that allow for blood vessels to reach the tendon.

• The sheath consists of visceral & parietal layer separated by synovial fluid. The fluid may stick & cause Tenosynovitis



• Bone building disease that affects one or a few joints.

( See ( radiodensity & ( Joint space of the joint involved due to Bone building activity

( Painful for the patient

• Some Non Inflammatory diseases:


|DJD |• Degenerative Joint disease used to be called osteoarthritis/osteoarthrosis. Although this is a non inflammatory |

| |disease, you will see secondary inflammation of the soft tissues |

| |• This is a reaction pattern to mechanical/biological factors |

| |( There is deterioration of the articular cartilage & formation of new bone at joint surface & margins. |

| |Older Women are more affected than men & it is common in Native americans. |

| |( In Males, DJD occurs below 50 due to occupation & high physical activity (large traumas) |

| |( Cellular changes occur as early as mid 20’s & by 40, 90% population have damage to weight bearing |

| |joints. |

| |( Most common form of joint disease in USA with 95% of population affected [NBCE]. Seen as we age |

| |& most common in weight bearing joints (ie: hip, knee, facets etc) |

| |(( We do not know the etiology but anything that damages articular cartilage can lead to DJD |

| |( Trauma (micro/macro), Inactivity, Infection, Collagen synthesis disorder, Subluxation, Nutrition & |

| |Genetics all contribute to DJD |

A. Factors that promote DJD:

• There are 3 major factors that are noted. These are:

- Genetic: Inherited poor cartilage that microscopically we can observe fibrillin that structurally weakens the cartilage.

- Injury: Anything can injure the cartilage but most often it is associated to trauma & to hypomobility. Here, also we have fibrillation.

- Subchondral bone stiffening: This is the result of microtrauma. Stiffening causes the cartilage to be put under even greater stress because the bone no longer does its part as a shock absorber.

B. Degenerative Events:

a) There is a combination of breakdown & buildup of bone & cartilage going on. The following events occur:

- Loss of chondrocytes - Fat deposition around chondrocytes

- Presence of fibrillation - Cartilage Erosion (due to cracks; leads to mice)

- Presence of matrix destroying protease (leads to softening of cartilage)

- Cartilage repair (mixture of hyalin & fibrocartilage)

b) Fibrocartilage formation:

• With severe & deep cartilage injury (down to BLUE line), we have fibrocartilage formation. Unfortunately, fibrocartilage makes a poor substitute for hyalin cartilage because it imbibes water & expands irregularly & is unable to absorb stress.

c) Osteophytes formation:

• There is new bone formation at joint margin that leads to exophytic growth (osteophytes). These osteophytes are contained within the capsule (some grow as much as 4 inches) & are guided by mechanical forces on joint. In reality, osteophytes are an attempt to repair & stabilize the joint by increasing the surface area & reducing the pressure on the bone. Osteophytes may also undergo degenerative changes & have osteophytes grow on them.

• In the vertebra, the osteophytes result from a tearing of the annulus at the periosteal attachment. With disc degeneration weight is shifted to the facets thereby ( DJD of the Facet joints. This may lead to spinal canal stenosis & IVF stenosis. [NB: WHEN YOU SEE OSTEOPHYTES ON THE RADIOGRAPH BE WARE THAT THE DISCS ARE ALSO PARTIALLY DESTROYED EVEN THOUGH THEY LOOK NORMAL ON THE RADIOGRAPH]

d) Subchondral bone formation:

• Subchondral bone will proliferate, especially where cartilage is reduced. The articular surfaces may be rubbed smooth (Eburnation) causing death of the osteocytes (Radiograph shows a white thickening of the subchondral bone). This may then lead to infiltration of the synovial fluid into the bone marrow area (geodes).

e) Other changes:

• Other changes include synovial villous hypertrophy (acids & enzymes produced excessively), capsular tears (pain) & ligaments/menisci become frayed and take a long time to repair.



C: Clinical & Radiographic findings:

( Clinically we see aching in region of joint (large area as per Hilton’s law). Pain is worse in the morning & worse at end of day. It is relieved by rest (but not prolonged rest). Activity can aggravate the pain. Crepitus (grating sound due to irregular surface) is heard.

( ROM is decreased gradually. Local swelling is evident (secondary to DJD process). Spinal cord & nerve root symptoms due to stenosing. Areas most affected are PIP’s & DIP’s with non symmetrical appearance from one side body to other.

( Radiographically, degeneration does not correlate with presence or absence of symptoms except in sever lumbar, hip or Knee DJD. The distribution is asymmetrical & there is non uniform loss of joint space with subchondral sclerosis evident.

( Radiographically we also see subchondral cysts, intraarticular mice, deformity, joint subluxation (partial dislocation) & a vacuum sign which is early degenerative sign due to release of Nitrogen gas around the vertebral disc.

D: Fun Facts:

• Removal of Menisci predisposes the knee to DJD. DJD will be Worse in the HAND (we don’t know why this is so). May also have DJD at hip, spine, ankle.

• Obesity is contributes to DJD because of the increase weight carried by the joints & lack of activity leading to ( ROM. ALL joints are affected.

• Ligamentous laxity predisposes to DJD because it leads to uneven wear ( uneven joint loading.

• Osteopetrosis leads to DJD due to bone getting stiffer & not doing its shock absorbing properly

• Acromegaly predisposes to DJD due to altered joint surfaces

• Running may or may not predispose to DJD. If running done correctly NO problem. However, if running not done correctly, it can lead to DJD.

• Barometric changes may lead to DJD (this is still being debated)

E. Treatment:

• Chiropractors can do the following:

- ( ROM, ( Pain - Recommend wt. loss/nutrition - ( muscle strength

- Recommend exercises - Ultrasound/diathermy/hotpacks - Nutritional supplements

- Wobble board - Suggest removing tripping hazards from home

• Medical doctors:

- Pain meds & steroids

• Orthopedic Surgeon:

- Joint replacement

• Other health care professionals:

- massage therapist - counsellors - P.T’s - nutritionist

- Acupuncturist - herbologist/homeopath



• This disease is associated with anterior knee pain (albeit an imprecise term that is all to often used as a Catch All diagnostic)

• What appears to happen is that the cartilage is softening & then fissuring followed by fibrillation (similar to DJD).

( Microscopically these changes are seen in almost everyone over 25 with 30-50% adults showing gross changes.

A. Causal Theories & Factors that promote CMD:

• Possibly due to inherent cartilage defects

• Abnormal contact with synovial membrane (( in synovium causes ( in enzymes & hyaluronic acid causing breakdown of bone)

• Loss of contact with articular cartilage (patella-femoral joint)

• Onset is associated with:

- jogging/repetitive loading - immobilization & casting due to fracture

- Improper appliances (knee braces) - Medial meniscecotomy

B. Degenerative Events:

• There may be abnormal function of extensor mechanism and/or parts don’t fit together properly. Often times there is recurrent subluxation/dislocation of the patella (patellar instability or damage)

• Cartilage needs to have pressure applied to it; however, too much or too little pressure can cause CMP by modifying calcification/vascularization of subchondral bone.

C. Clinical & Radiographic Findings:

• Age of onset is 16-30 ( insidious w/out recent trauma) with ratio between males/females equal.

( Patient has a diffuse ache in one or both knees that is fairly constant & made worse by activity & stair climbing.

( Squatting may be impossible with grating sensation on load bearing. (family history seems to be present)

D. Treatment of CMD:

• Chiropractors can offer the following:

- Long axis distraction - Adjustments - Recommend physical activity

- Orthotics - Muscle issues

• Medical Doctors can:

- Pain meds & refer to P.T.

• Orthopedic surgeon can:

- carry out patellar resurfacing by scraping away the cartilage past the BLUE LINE & then cartilage replaced by fibrocartilage


• AKA neurotrophic arthropathy, neuroarthropathy or Charcot’s joint

• This is a destructive articular disease secondary to Neural damage

• Patient experiences premature & excessive traumatic degeneration resulting in severe destruction & instability of the Weight bearing joints especially knee & ankles

( Patient doesn’t feel much due to the Neuropathic issues.

A. Factors that Affect Neuropathic Arthropathy:

• May be congenital

• Acquired (most common is with uncontrolled diabetes, but can also be due to infection, trauma to a nerve, Multiple sclerosis)

• Iatrogenic (physician induced)

B. Clinical Features & radiographic findings:

( Mostly seen in ankles, feet & knees producing altered gait

( Patient has loss of Deep Tendon Reflexes (DTR)

( Patient is insensitive pain which further leads to degeneration of joint

( The problem can occur in weeks, months, or years

( Radiographically we don’t see much initially (only the nerve is injured). Later we have DJD, Dislocation & debris (bag of bone appearance)

C. Treatment:

• First address the primary cause & provide support/education for the patient.

• If destruction is severe, amputation may be required.



• Bone destroying activity is occuring at many bones with osteopenia very evident

( See ( radiodensity & much bone erosion with soft tissue involvement

( Subluxations/Partial dislocations are very common

( Painful for the patient


• This is a systemic inflammatory disease affecting the skin, blood vessels, muscles, heart, lungs & mostly the joints

( Joint pain is only the tip of the iceberg as the vascular compromise can be more serious

• Rheumatoid arthritis is not “Rheumatism” which is a term used in olden days to refer to DJD

A. Description & Degenerative Process:

• RA is a non suppurative proliferative “synovitis” (inflammation of the synovium) leading to articular cartilage destruction & ankylosing of the joints involved.

• The synovium goes from being a few layers thick to 1000’s of layers thick. This increase causes release of lysosomal enzymes & hyaluronic acid that destroys the cartilage & also prevents nutrition from diffusing into the cartilage.

( It occurs in about 1% of population & affects females more than males (3.5-1) generally being diagnosed in mid 30’s. Etiology is unknown but virus, autoimmune & genetic causes are being looked at.

• The disease is highly unpredictable with onset being gradual for 90% of patients.

( Greatest damage occurs within first 5 years & damage is worse with older age of onset

( Etiologically begins as a non distinct inflammation where the synovium becomes edematous, thickened & hyperplastic (helper T cells, plasma cells & macrophages are commonly seen deposited in areolar tissues).

( This is followed by fibrin covering the synovium (often fibrin break off as RICE BODIES).

( Then we have synovial thickening called PANNUS with Villi production. The pannus fills in the joint space producing proteases, elastases & collagenases with inhibition of proteoglycans.

( Inflammatory cells (PGE2) stimulate osteoclastic activity & bone margin (juxta articular) erosion occurs with possible subchondral cysts. A typical “Rat Bite lesion” will be seen at bone margin & Juxta articular osteoporosis sets in.

( The immune complex RA-IgG is present & attacks the collagen & blood vessels. We then see a Type II autoimmunity set in.

( There is continued fibrous tissue development that leads to fibrous ankylosis & finally Bony ankylosis (rarely occurs as most RA stops at Fibrous ankylosis)

(( The tendons/ligaments may rupture due to increase in enzymes within the ligaments.

B. Clinical Presentation:

• It generally affects the smaller joints first & then moves on to the larger joints. Most common area is Hands, Wrists, feet (will also affect ankles, knees, elbows, hips & shoulders). Involvement is SYMMETRICAL & MCP’s/PIP’s most often affected.

• Spine is not normally involved (if found it will be in the cervicals)

( Patient will present with malaise, fatigue, low grade fever & non localized musculocutaneous pain.

( The joints will become red, swollen & very painful with stiffness during & after activity

( 25% of patients develop rheumatoid nodules (mostly in severe cases) around the elbow & forearms. These nodules are areas of fibrous necrosis with lymphocytes & granulation tissue.

( Some patients have non specific conjunctivitis (often both eyes) & acute “vasculitis” in the more severe cases. This vasculitis can lead to gangrene in worst case scenario.



C. Lab & Radiographic Findings:

• Lab results are used to support the diagnosis & should not be used to make a diagnosis from.

• ESR may be elevated & “Waxes & Wanes”

• Alk. Phos. is normal

• Bone scan will show slight elevation due to bone repair going on.

• Plain films will be normal in the early stages.

• Patient may have mild anemia due to immune complex hanging onto the RBC’s (not iron deficient anemia)

• Rheumatoid Factor (RF) is present. It is a complex of multiple antibodies; primarily IgM against IgM fragments. A patient with RF in blood test is termed “Seropositive” & seen in 90% of patients with RA. Some patients show RF+ but do not have RA

( Radiographically disease presents with bilateral symmetry & has periarticular soft tissue swelling.

( We see Juxta-articular osteoporosis (loss of bone density due to disuse & enzymes, PGE2)

( Joint space loss is uniform & we see RAT BITE lesion at Barre area of bone

( Pseudocysts form that fill with PANNUS

( MTP & PIP dislocate & deviate laterally due to strength of muscles & MCP ulnar deviate. Wrists go radially & fingers flex.

( Transverse ligament in cervical spine may erode leading to cervical instability

D. Treatment:

• Chiropractors can advise on diet & exercise (water aerobics, & finger extension exercises). Adjust when not inflamed & keep joints mobilized when inflamed. Most of spine is not involved so we can adjust it quite well.

• Supplements such as Glucosamine sulfate, Omega 3 Fatty acids & reduce animal products while staying away from “nightshade” family of plants

• Medical Doctors can prescribe for pain relief (NSAIDS, Steroids, Cox2 RA inhibitor, methotrexate, Gold salts injections.

• Orthopedic surgeons can replace joints or fuse into acceptable position some joints (ie hands)

• Other practitioners are homeopaths, occupational therapists, acupuncturists, massage therapist


• Maybe called Still’s disease or Juvenile Arthritis [NBCE]

• Occurs in younger than 16 year olds

• Although changes are similar to adult RA, there is less inflammation & pannus formation

A. Description & degeneration process:

• May cause growth plate disturbances by accelerating activity & cause premature fusion of growth plates

B. Clinical Presentation:

• May be mono, oligo or systemic involvement & is NOT always Bilateral.

( It is migratory & transient from Joint to Joint (knees most often affected)

( Rash, Fever & organ enlargement & not always involvement of heart, liver, spleen or vasculitis

( 70-90% of patients have complete remission

C. Treatment:

• Chiropractors can advise on diet & exercise (water aerobics, & finger extension exercises). Adjust when not inflamed & keep joints mobilized when inflamed. Most of spine is not involved so we can adjust it quite well.

• Supplements such as Glucosamine sulfate, Omega 3 Fatty acids & reduce animal products while staying away from “nightshade” family of plants

• Medical Doctors can prescribe for pain relief (NSAIDS, Steroids, Cox2 RA inhibitor, methotrexate, Gold salts injections.

• Orthopedic surgeons can replace joints or fuse into acceptable position some joints (ie hands)

• Other practitioners are homeopaths, occupational therapists, acupuncturists, massage therapist



• There are 4 in this category: - Ankylosing Spondylitis - Psoriatic Arthritis

- Reiter’s Syndrome - Enteropathic Arthropathy

• They are generally Seronegative, affecting mainly the spine & with asymmetrical involvement

• Few peripheral joints are involved (although this is untrue for Psoriatic arthritis where the majority of problem involves distal joints)

• Often seen in younger males between 15-35 years of age & the HLA-B27 antigen will be present most often


|Ankylosing Spondylitis |• AKA Rheumatoid Spondylitis or Marie Strumpell Disease [NBCE] |

| |• Mainly affects the spine and only 1/3 patients have peripheral joint involvement. It is quite common & seen |

| |more |

| |in males than females |

| |• Generally appears around 15-30 yrs of age with diagnosis around 23. (sibling 20% chance of getting it) |

| |• Etiology is unknown but Autoimmune is possible |

| |• Synovial joints develop a Pannus & Cartilaginous joints develop granulation tissue. Essentially the ligaments|

| |ossify (spinal ligaments almost always involved). There is local ligament inflammation with reactive bone |

| |formation at end of ligament/tendon (enthesopathy) |

| |( There may or may not be pain initially. Patients note loss of ROM & general stiffness that is worse at night |

| |( Always begins at SI joints then works its way up the spine. Patient demonstrates an increased Kyphotic curve |

| |( Lab findings: ESR (, Alk Phos normal, RF-, HLA B27+, RBC (, Bone scan ( activity |

| |( radiographic findings normal in early stages but progressively show the following signs: |

| |- Bamboo spine - Dagger Sign (supraspinous ligament ossifies) - Trolley track sign |

| |(facets fuse) |

| |(Syndesmophytes is ossification of ALL, PLL & annulus |

| |( Chiropractors adjust areas that are not locked up & keep up ROM. Suggest diet & acceptable activity |

| |( MD give pain relief NSAID’s. Orthopedic surgeons can do little unless fractures present |

| |( Other professions same as in RA |

| |( AS may present in Children & is not common. It occurs in late childhood with SI findings but spares hands, |

| |wrists & C spine. ( Lab Tests are RF-, HLA B27+ |

|Psoriatic Arthritis |• Occurs in only 10% of patients with Psoriasis. |

| |• Psoriasis develops btwn 10-30 yrs age & arthritis appears btwn 20-40 yrs age |

| |• Psoriasis has abnormal keratinocyte proliferation (normal 21 days; psoriasis 3 days) |

| |( Skin lesions on extensor surfaces, knees & scalp. Skin flare ups may precede ( joint symptomatology |

| |( Patient may have skin lesions, Finger/toe nails show pitting (20 pits suggestive, 60 diagnostic) |

| |( Similar to RA in presentation however mostly extremity involvement with uneven distribution (30% patients |

| |have TMJ problems) & some have atlantoaxial instability |

| |( Lab tests show ( ESR, RF -, HLA B27+, Alk.Phos normal, Leukocytes ( & RBC ( (anemia) |

| |( Radiographically soft tissue swelling with “Sausage digits”. Bone density is normal but erosion of bone occurs|

| |leading to Telescoping of digits. |

| |( Joint space narrows uniformly & “fluffy” periostitis around bone margin |

| |((Pathognomic sign is “MOUSE EARS OR PENCIL IN CUP”. Some patients develop spinal ankylosis, but |

| |with less obvious pattern than AS itself |

| |( Treatment is the same as for RA & AS |

| |( A Juvenile PSA exists affecting ages 9-12 females more than males with similar skin, nail & sausage digits |

| |(hip |

| |involvement less common) |

|Reiter’s Syndrome |• Identified by a Triad of Symptoms: - Arthritis - Conjunctivitis - Urethritis |

| |• Most common in young males (20-30’s) with predominance in military populations |

| |( Onset symptoms 1-4 weeks after venereal exposure or dysentery (shigella) with Urethritis being first symptom |

| |(although diarrhoea may precede urethritis) |

| |( Conjuctivitis is mild & bilateral & may last days/weeks but is self limiting |

| |( There may be a painless rash on palms, soles & oral mucosa which may later become superficial ulcers |

| |( Asymmetrical arthritis involving knees, ankles, achilles tendonitis & SI joints |

| |( 2/3 patients never have any other episodes but 1/3 progress to arthritis with most only showing 2 of 3 |

| |symptoms |

| |( Lab tests show ESR(, HLA B27 (, RF negative |

| |( Rest because it is self limiting. Topical corticosteroids & refer to ophthalmologist to prevent blindness |

|Enteropathic Arthritis |• It is associated with Ulcerative colitis & Crohn’s disease affecting 1 major joint at a time. |

| |• It is migratory & stays in the peripheral joints & subsides within six weeks (although may reoccur later in |

| |life) |

| |( Often preceded by diarrhoea |

| |( Cause is not known. Suspect microorganisms, “leaky gut” or Autoimmune [NBCE] |

| |( Milk often aggravates the condition with intestinal symptoms preceding arthritis attacks |

| |( Antibiotics, Bowel resection in ulcerative colitis & symptomatic management |



• The great mimicker because it presents like the following diseases:

- Lupus, HIV, Flu, RA, MS, EBV, Reiter’s, meningitis, Clinical Depression, Multitude of infections

( Early symptoms are:

- Variety of rashes with “Bullseye pattern” common, Fatigue, Headache, Neck stiffness, Jaw discomfort, Pain/stiffness in muscles & joints, Slight fever, Swollen glands, conjunctivitis

( Later symptoms are:

- If untreated, there are heart, nervous system or joint complications. Most common is joint pain & swelling that is migratory & transient. The pain may occur from one to many months after the bite. Movement is painful but there is minimal cartilage/bone damage

- Heart symptoms may occur within 1-3 weeks after rash with dizziness, weakness & irregular heart beat

- Nervous symptoms are seen 1 month after onset of disease. There are intermittent headaches, difficult sleeping/concentrating, neck stiffness ( SCM/Traps)& poor motor coordination. Later on there is paresthesia of extremities, weakness in arms & legs & depression

( Heavy duty antibiotic cocktails


• A multisystem immune disease that affects skin, joints & kidneys (may be life threatening)

• Affects females moreso than males & in black females with age of onset teens - 40 years age

• Etiologically may be due to genetics but some medications have induced SLE. UV light may trigger SLE

( We see deposition of immune complexes & fibrinoid materials in small arteries & arterioles with necrotizing vasculitis (blood vessels thicken & narrow)

( The skin is red with butterfly rash over bridge of nose. Sunlight accentuates the lesion that may appear on neck, elbows & dorsum of hands.

( Kidneys may have glomerular damage with renal failure leading to death

( We may also see alopecia, acute vasculitis of serosal membranes that ulcerate & in 90 % cases Joint involvement (non erosive synovitis)

( Joint are involved bilaterally & symmetrically (often hands, knees, wrist & shoulders) swelling & painful like RA with reversible subluxation in hands. [ATLANTO AXIAL INSTABILITY]

( Condition presents as a self limiting rheumatic disorder with symptoms of malaise, fever, anorexia, weight loss, polyarthralgia, & skin rashes. Tendons may rupture spontaneously.

( Corticosteroids to keep inflammation down, but then patient takes on weight

( Adjust non affected joints but watch out for C1



• Discussed here are Gout & Psuedogout.

• Gout has deposition of Sodium Urate Crystals only

• Pseudogout has many types of crystal depositions; all of which do not include Sodium Urate crystals


|Gout (AKA Gouty Arthritis) |• The crystalline deposition may occur anywhere in the body. |

| |• IN gout we have Sodium Urate crystals deposited & an elevated uric acid level in the blood, |

| |due to overproduction or inability to dispose of the byproducts. |

| |• Primary gout is seen in 1/3 of patients (w/out any other precipitating factors). The remainder|

| |2/3 |

| |have underlying pathologies. |

| |( This is seen in 2% of population & affects Males more than females because Males produce |

| |more uric acid than females at baseline. |

| |( We see Hyperurecemia, recurrent attacks (principally 1st MTP) with remission. |

| |(( Tophi (cheesy, milky,deposition) occurs in soft tissues primarily in fingers, toes, & ears. |

| |These are Pathognomonic of GOUT |

| |( 90% have acute arthritis of 1st MTP called PODAGRA that is red, hot swollen & occurs |

| |overnight, waking the patient up around 2-3 am. (the weight of sheets wakes them up due to |

| |pain). This condition if untreated remisses in one week but may re-occur in the future |

| |( 10-15% patients develop chronic gout with TOPHI . Moreover, there is PANNUS formation |

| |with destruction similar to RA & possible renal involvement as crystals deposit in kidneys |

| |( We know that stress (physical, emotional & alcohol) may precipitate gout |

| |( Chiropractors can correct diet (remove red meats, Asparagus & wine), proper exercises, adjust |

| |non affected joints & warm affected joints (in early stages) to break down the crystals) |

|Pseudogout |• One example is Calcium Pyrophosphate Dehydrate crystal deposition (CPPD). May present as |

| |Primary (no other reasons) or Secondary (other problems: Diabetes or Wilson’s) |

| |( Clinically it may look like Gout, RA, DJD or NA |

| |( Crystals deposit into cartilage, synovium, tendons & ligaments |

| |( However, onset is around 30 yrs & peaks at 60. There is chronic progressive joint pain with |

| |( ROM & crepitus affecting the peripheral joints (esp. knees, wrists, hands) |

| |( We treat as for DJD. M.D.s give steroids & NSAIDS |



|Septic Arthritis |• May occur at any age but most often in infants/children because their immune system is still |

| |under development |

| |• Microorganism gets into joint by: Hemotogenous spread, Implantation or Direct extension |

| |• The most common culprits are: S.aureus, H.influenza & gonococcal (sexually active adults). The|

| |bacteria take sup residence in synovial membrane & inflammation causes PANNUS |

| |(( Acute form can progress in 48 hours to serious state with irreversible damage within 1 |

| |week. The joint is swollen, red, hot painful. It may also become chronic & have flare ups |

| |occasionally. |

| |( Usually larger joints involved & monoarthritic. The Lab tests show: |

| |- ESR ((acute, normal Chronic) - Alk Phos (normal) - HLAB27 (-) |

| |- RF (-) - Synovial Biopsy (+) |

| |( Treatment is antibiotic & aspiration to decompress the joint. Decrease motion & weight |

| |bearing to prevent damage to cartilage |

|Fungal Arthritis |• It is a RARE occurrence & often due to complication of neoplasms because of weakening of the |

| |Immune system or in AIDS patients |

| |( Often associated with Primary lung & athletes foot. It is highly destructive & difficult to |

| |TX. If |

| |it occurs in the spine it resembles POTT’s disease |

| |( Diagnosis by biopsy & treat aggressively |



a. General Information:

• The skeletal muscles are named from largest unit to smallest (named muscle(Fasciculus(Muscle fibre cell( Myofibril ( Sarcomere( Myofilaments)

• Muscle surrounded by Epimysium

• Fasciculus surrounded by Perimysium

• Muscle fibre surrounded by Endomyseum

b. Cell Structure:

• The muscle cells are long & multinucleated & enveloped by a Sarcolemma that is thin, elastic & non cellular.

• Presence of the myofibrils gives striated appearance to muscle.

• A Sarcomere is a contractile unit of myofibrils

- Contains 1/2 of two I bands, Central A band, H zone & M Line

- Thin filaments (each being equidistant from 3 thick filaments) form hexagon around each thick filament

• The sarcoplasm (AKA sarcoplasmic Matrix) is a fluid containing myoglobin, glycogen & Fat droplets, phosphate compounds & other small molecules ions. Myofilaments are embedded in sarcoplasm.

• The Sarcoplasmic Reticulum (SR) is part of Sarcoplasm & regulates the Ca++ ion flow ( this Ca++ has nothing to do with blood/ECM Ca++)& surrounds each myofibril. Terminal Cisterne of SR approximate T tubules & form a TRIAD. When Depolarization occurs the SR passively releases Ca++ into cell (when stimulus is stopped Ca++ goes back into Cisternae).

• The Thin Filaments are composed of 2 major proteins (Actin - globular & Tropomysin - rod shaped). Actin monomers twist together in a helix fashion. Tropomysin form together as a helix & are associated with 6-7 actin monomers. Tropomysin lie end to end within the actin helix groove.

• Troponin is the most important regulatory protein & is a small globular protein linked to one end of the tropomysin molecule. It is composed of TnT (attaches troponin to tropomysin), TnC (binds Ca++) & TnI (inhibits actin-myosin interaction)

• The Thick Filaments is called Myosin & made up of 6 different polypeptides & 1 tertiary globular protein (make the head of myosin). Myosin can be divided into one set of heavy chain proteins & two light chain proteins (genetically different for different muscles. ie: fast/slow twitch). Myosin aggregate to form thick filaments with heads each separated by 60( & stick out of the bundle. The heads moreover, align in a hexagonal fashion.


• Muscle length occurs by the sliding of actin/myosin filaments. However, the length of the filaments remains constant.

• A “Cross Bridge” cycle has 4 steps: Rest, Excitation, Contraction, Relaxation

• With each depolarization 1 single crossbridge cycles thousand’s of times.

a. Mechanical aspect:

• At rest no interaction between Actin/myosin occurs because the tropmyosin/troponin complex blocks the binding site. Resistance to passive extensibility is modest.

• During excitation the AP depolarizes cell through the T tubule & SR becomes permeable allowing the Ca++ into sarcoplasm.

• An excitation-contraction coupling is process by which depolarization initiates contraction. Electrical signal converted into mechanical action. Ca++ binds to the TnC. CALCIUM IS THE KEY TO IT ALL.

• Contraction occurs when the Ca++ binds to the TnC & then changes the Troponin-Tropmyosin complex allowing the actin binding site to be exposed. Myosin heads move towards the actin binding sites & then pull the actin filaments along.



b. Energetic aspect:

• At Rest, ATP is bound to the Myosin head & ATPase converts ATP into ADP-Pi form preparing it to bind with Actin (change is conformational only & doesn’t involve hydrolysis).

• With Excitation , Ca++ is released into the cell & binds with TnC, allowing the Actin Binding Site to be exposed to the “Primed” Myosin heads. ACTOMYOSIN Complex is formed (new protein complex).

Then, Actomyosin ATPase breaks Adp & Pi) apart (releasing them into the sarcoplasm) liberating energy & then myosin head pulls Actin across the myosin fibres. Next, the liberation of ADP & Pi allows the ATP binding site on Myosin head to open allowing ATP to attach & release the Myosin head from the Actin.

The cycle is repeated as long as the depolarizing event continues & ATP is present. With stoppage of Depolarization, Relaxation begins.

( If no ATP present (as in Rigor mortis) Ca++ leaks out & binds to Troponin C & cross bridges from. However after some time ATP itself degrades & there is a gradual release & Rigor Mortis disappears.

• Relaxation occurs when Ca++ is pumped back into the SR. As this occurs Troponin/tropomyosin complex block the Actin binding site.

• The SR consists almost entirely of pumps having Ca++ affinity & through Active transport 2 moles of Ca++ are sequestered per mole of ATP hydrolyzed.

• Calsequestrin is a Protein within the SR & one mole of it can bind 43 Ca++ ions. Because Calsequestrin reduces the Active Transport Gradient it helps move Ca++ into the SR.

c. Summary:

• Calcium is essential factor between Excitation & Contraction of Skeletal muscles

• On Board Ca++ does not change with variations in Extracellular Ca++. However, as Extracellular Ca++ changes it affects the Nervous system & causes a change in muscle activity.

• The Action of crossbridges is to exert a Longitudinal force over a distance thereby moving the Actin over the Myosin.

• When Ca++ is moved back into the SR the process is Switched OFF.


a. Mechanical Variables in Contraction:


|Force (F) |Newton (n) |

|Length (L) |Meter (m) |

|Time (T) |Second (s) |

b. Derived Variables:


|Velocity (V) |Change in length/change in time |

|Work (W) |Force x Distance shortened |

|Negative Work (-W) |Force x Distance lengthened |

|Power (P) |Work/Time |

|Stress (S) |Force/cross sectional area |



c. Length-Tension (AKA Length-stress curve):

• Active stress (tension) is proportional overlap btwn thick & thin filaments ( stress (tension) is the proportional number of active crossbridges that interact with the thin filaments

• Muscles have an optimal length where maximum force can be developed & Stress ( linearly with overlap btwn Actin & Myosin

• At the Peak of the L-T curve, we have a small area where tension doesn’t change with length (see pg 3). Force declines at less than optimal Sarcomere lengths (lower tension due to control mechanisms being less sensitive)

This can be understood by thinking of Nautilus gym equipment; little load is applied when muscles are fully stretched or fully contracted. This is done through a Cam mechanism.

d. Force-Velocity:

• With very short sarcomere lengths, cross bridges must attach / detach asynchronously. Crossbridging occurs at various rates depending on the imposed load (ie: like a bike with gears)

• Shortening velocities of muscles depend on:

- Number of sarcomeres in a Cell.

- Load on the muscle. Crossbridge cycling decreases as Stress (tension) increases (see pg 5 graph)

- Physiological differences in Myosin head such as ATPase, construct of light chain proteins (genetically different muscles)

e. Muscle Contraction:

• The Amount of Ca++ released determines the contractile response of the System.

• SR releases the Ca++ when the membrane potential is less Negative than -50 mV (AKA mechanical Threshold)

Maximal Ca++ release occurs at -20 mV

• The Ca++ pulse may be increased by lowering mechanical Threshold, Prolonging the Action potential.

• Although a Single AP is capable of activating the contractile machinery, the Ca++ is rapidly pumped back into the SR before the muscle develops maximum force. (This is known as a Twitch & may not be detectable by eye)

• Repetitive AP’s cause a summation of twitches producing partial or complete tetanus (see pg 7). A number of crossbridge cycles must occur before maximal force is registered at the Tendons (due to the elastic nature of muscle elements & the muscle actually lengthens first when it is loaded up)

• This stretching is termed “Series Elastic Component” & once the “stretch” is removed all subsequent contractile effort will begin to contract the muscles. (see graph pg 9)

• Excised muscles can be stimulated electrically, chemically or mechanically. On Non excised muscles we can stimulate them by EMG, Chemically (motor neurons) or mechanically (bruising).

f. Types of Muscle Contractions:

• A Myogram records muscular events & consists of:

- Latency period - Contraction phase - relaxation phase

• The length of the phases depends on the type of muscle being contracted & the type of contraction used

• A Dynamic (shortening contraction/concentric contraction) has a muscle origin moving towards its insertion. The muscle moves through acceleration, constant velocity braking phases (tension varies in each phase)

• An Eccentric (lengthening contraction) has a muscle contracting but origin & insertion move away from each other.

• An Isometric (same length) contraction has tension build up without visible shortening of muscle & therefore origin & insertion are fixed

• An Isokinetic (a true isotonic) contraction has the muscle shortening at a constant velocity. (only occurs with experimental instrumentation use (Biodex machine)



a. General Information:

• Muscles are not homogenous tissue; being made up of fires of varying mechanical & contractile properties.

• There are two classes of muscle fibres:

- Type I (slow twitch/Red fibres)

- Type II (fast twitch/White fibres). These are subdivided into Type IIa (intermediate) & Type Iib

b. Determiners of Fibre Type:

• Classification is based on ATPase, myosin composition, troponin structure, Amount of SR, mitochondria & metabolic characteristics.

• Moreover, genetic makeup plays a role with fibre differentiation occuring around wk 20 in utero (differentiation is almost complete by 1 year of age)

• There is good support showing that the Nervous System plays a big role also.

- Motor neurons innervating the Type I fibres are smaller & have slower conduction rate when compared to Type II.

- Studies have shown that cross inervation of muscles will cause the muscle to take on the characteristic of the Neuron innervating it.

- Studies of electrical stimulation of muscle shows that Type II fibres transform into Type I easily. It is harder to transform a Type I into a Type II.

c. Modifying Metabolic Profile:

• Training can affect the muscle fibres. Endurance training ( [ ] of mitochondrial enzymes as well as their quantity & volume in ALL fibre types

d. Recruitment:

• When motor units in a muscle progressively activate in a Graded Contraction this is known as Recruitment.

• Low threshold units are recruited in mild sustained contractions with a frequency of 5-10 Hz.

• As Contractions increased discharge rate increased to about 25 Hz

• So initially we have Type I fibres firing mostly. The Type II fibres only fire during Rapid (ballistic) movements & in this case the Type I fibres are mostly silent.


a. Strength Training:

• The maximum tension that a muscle can produce depends on its total Cross sectional area.

• Strength training can be done by:

- Hyperplasia: an increase of number of fibres (does not occur in humans)

- Hypertrophy: an increase in the diameter of existing muscle fibres (happens in humans)

• In strength training both Type I & II fibres hypertrophy (Type II moreso than Type I because they are recruited first)

• Factors determining Strength are:

- Differences in Bony leverages (shorter the better) - Co-ordination

- Motivation of individual - Age (may help elderly with co-ordination)

b. Endurance Training:

• Primarily done to increase resistance to fatigue of muscles involved by:

- ( capacity of fibre to produce ATP thru Oxidative Phosphorylation

- ( capilarization

- ( myoglobin content

- ( mitochondrial number & enzyme [ ] in muscle (Occurs in type I more than in Type II)

( There is some belief that Type II a fibres can be converted into Type I fibres

• Other factors affecting endurance are:

- Cardiovascular system efficiency - Motivation - Age

c. Atrophy:

• Disuse of muscles can cause them to Atrophy with loss of myofibrils, ( in mitochondria & other structures

• Type I fibres atrophy much quicker than Type II during short terms of inactivity (ie as in a cast)

d. Training; One last thought:

• Metabolic differences in potential to perform aerobic/anerobic exercise is question of habitual use/disuse

• Genetic endowment specifies neural component & the proportion of muscle fibre types



a. Hallmarks of Muscle Pathology:

( Atrophy & paralysis with weakness (easily fatigued & stiff muscles) & cramps.

( Patient may have co-ordination issues. There may also be secondary loss of bone density

b. Neurological VS Muscular Pathology:


|Affects extremities on one side only & often localized |Affects more proximal sites (pelvic/shoulder girdle muscles) |

|More distal involvement due to greater nerve distance travelled |Fatigue under activity |

|MRS, Muscle tests, Reflexes & Dermatomes will all be affected | |


a. Duchenne Muscular Dystrophy (DMD):

• All muscular dystrophies have the following characteristics:

- Degeneration of muscle fibres - Regenerative activity (albeit not as it should be)

- Progressive fibrosis of the muscles - Infiltration of Fatty tissue (particularly with Duchenne’s)


• The most severe & rapidly progressing dystrophy with a Genetic origin affecting Males (3:100,000 births). 2/3 of patients have relatives with DMD & 1/3 due to mutation

( Abnormal muscle morphology is witnessed in Utero with an Elevated Creatine Kinase from Birth. Child begins to have problems around 3-4 years of age (difficulty standing). By 10 years they are wheelchair bound, 15 bedridden & 20 death due to respiratory insufficiency

( A peculiar symptom is “Pseudohypertrophy” of the Muscles due to Fat/Fibrosis building up in the tissues

b. Rhabdomyolysis:

• This is a Diffuse destruction of skeletal fibres of unknown cause. It presents with clusters of macrophages in & around the muscle fibres. IT is NON INFLAMMATORY.

( May have acute presentation where there is excessive sarcoplasmic contents put into circulation causing Myoglobinuria that can lead to Acute Renal Failure.

( Patient complains of swollen, tender muscles with profound weakness & often follows one of the Following:

- Flu - Mild exercise (strenuous exercise no problem) - Heat Stroke -Alcohol Intox.


a. General Information:

• These are rare conditions that arise from an autoimmune disorder & associated with CT diseases

• Most often there are problems with the use of proximal muscle groups & swallowing difficulties.

( Both serum CK & ESR will be raised.

( Although exercise has been discouraged, now it appears to be beneficial for the following reasons:

- ( muscular strength - ( cardiovascular performance - No ( in CK noticed

( Corticosteroids work well for all but the Inclusion Body type of Inflammatory myopathy.

Chiropractically we could adjust & also possibly use Pulsed ultrasound (creates no heat in tissues)



b. Dermatomyositis:

• Occurs in adults as well as children affecting Females moreso than males. It isn’t really a muscle problem as there is a compliment antibody that attacks microvasculature of the skeletal muscles causing ischemia of the individual fibres

( There is infarction & secondary inflammation with skin involvement (redness of skin). The muscle fibres are atrophied & blood vessels are damaged.

( 15-40% 5 year death rate depending on where Treatment is sought

c. Polymyositis:

• Generally occurs after 20 years of age & is due to T cells damaging the Muscle fibres directly. Unlike Dermatomyositis there is no Microangiopathy.

( There will be necrosis, phagocytosis, regeneration & fibrosis. Patients with HIV have a similar pattern of muscle inflammation & often the degeneration is not in the area of inflammation

d. Inclusion Body Myositis:

• More often seen in males than females, occuring after 50 yrs age with damage being done again by the T cells.

• There is presence of a specific antigen on the sarcolemma.

( There are granular inclusions (of unknown origin) in the cytoplasm & or Nuclei of involved muscle fibre


a. Periodic paralysis:

• This condition exists in varying degrees & may show as a mild weakness or worse. (do not confuse with hysterical paralysis of psychological/emotional nature.

• It is Due to an Inherited Potassium metabolism problem & runs in families & there are 3 distinct classes:

1. Hyperkalemic (( potassium):

• The attacks last less than 1 hour & aggravated by exercise

2. Hypokalemic (( potassium):

• Begins in young adults & improves with age. Patient has general weakness of voluntary muscles

3. Normokalemic:

• Has a genetic predisposition & symptoms may last days or weeks

• Muscle biopsy taken at various sites in the body will come up negative btwn attacks

• It is believed to be caused by muscle surface not allowing the propagation of the Action potential. However, Calcium in the muscle results in contraction of muscle

b. Myositis Ossificans:

• This is a muscle pathology that converts muscle(sometimes also fascia, tendons, joint capsules & fatty tissues) into bone. Existing bones may look mores dense du to ( density of soft tissue. There is nothing wrong with the existing bones.

• It is a process that requires 3 stages as follows (occuring after trauma):

1. Pseudosarcoma (4-6 weeks):

• Necrosis, degeneration, regeneration, cellular proliferation with poorly defined cells. Sarcolemma begins to leak & fluid accumulates near central area (phagocytes make holes even larger).

• Tissue is liquefied & replaced by non specific cells

( Massage, stretching, surgery, excess activity & ultrasound can aggravate the problem

• After 15 days there is proliferation of mesenchymal tissue with minimum osteoid formation (looks like a neoplasia & can be confused for a Osteosarcoma)

2. Differentiation (2-3 months):

• Mesenchymal cells differentiate into chondroblasts, fibroblasts & osteoblasts with giant cells removing debris. Begins its mineralization process on the outside moving in. Centre can remain fluid filled with undifferentiated cells.

3. Maturation ( ?Long Time?):

• Periosteum develops that separates it from the surrounding tissues. It can stay like this for ever, shrink & disappear or if need be surgically removed.

c. Myositis Ossificans (with Neurological Disease):

• There is nervous system disruption & may be seen in the brain, cord or peripheral nerves. Pathology develops distal to neurological lesion & relationship is as yet unknown.

d. Progressive Myositis Ossificans (non trauma Induced):

• Extremely rare with symptoms beginning around 2 yrs or by adolescence, involving muscles of the back & major joints

• Muscles ossify progressively & severe functional disability occurs with death due to loss of pulmonary function


Cartilage is avascular & therefore produces Type II Collagen.

All other tissues have Oxygen & therefore produce Type I Collagen




bo ne

bo ne

Tears & splits here.

Most seen in kids

Fracture spirals around the bone


PTH Primary action is to raise Ca++ levels & secondary action is to decrease Phosphate levels by acting on Bone, Gut & Kidney


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