1. Orthopaedic -Osteoarthritis
Articular cartilage = has
Matrix which consists of a proteoglycan ground substance that contains
Collagen network and chondrocytes .
Compressibility and elasticity .
Fibrillation of articular cartilage.
OA = is a chronic joint disorder in which there is progressive
softening and disintegration of articular cartilage accompanied
by new growth of cartilage and bone at the joint margins
and capsular fibrosis.
Although there are sometimes local signs of inflammation =it is not primarily an inflammatory disorder.
It is not a purely degenerative disorder ,although degenerative arthritis
term sometimes used for OA . It is dynamic process ( destruction and repair).

2. 2 Etiology = 1-Age = cartilage does age showing =
-diminished cellularity
-reduced proteoglycan
concentration
-loss of elasticity
-decrease in breaking strength.
NB.=these changes are restricted to certain joints and to specific areas of those joints, while other areas show little or no progression with age.
2-Primary changes in cartilage matrix = e.g. crystal deposition disease
and genetic defects in type 2 collagen.
3-Previous inflammatory disorders that might cause articular cartilage damage= enzymes released by synovial cells and leucocytes can affect proteoglycans , e.g. Secondary O.A can occur in patients with rheumatoid arthritis.

3. 3
4-In the majority of cases the precipitating cause of O.A is increased mechanical stress in some part of the articular cartilage =
This can be due to = a-increased load e.g. In deformity or instability
b-changes in the subchondral bone =can change
the shape of the articular surface or can reduce
the shock absorbing effect of the supporting
cancellous bone by increasing bone density.
So O.A can be primary when on obvious cause is found or can be
secondary to previous abnormality.

4. 4
Pathogenesis =
The earliest changes are an increase in water content of the articular cartilage and easier extractability of the matrix proteoglycans , this is due to failure of the internal collagen network that normally restrains the matrix gel.
At slightly later stages there is loss of proteoglycans and defects appear in the cartilage.
As the cartilage becomes less stiff secondary damage to chondrocytes may cause release of cell enzymes and further matrix breakdown.
When the articular cartilage loses its integrity ,there will be more force on the subchondral bone and so there will be focal trabecular degeneration and cyst formation.
There will be increased vascularity and reactive sclerosis in the zone of maximal loading.
Cartilage at the edges of the joint still has the activities of growth and endochondral ossification giving rise to osteophytes.

7. 7 Prevalence = O.A is the commonest of all joint diseases.
Autopsy studies show O.A changes in everyone over the age of 65 years.
Men and women are equally affected but more joints are affected in women than in men.
O.A changes are much more common in some joints = fingers ,hip , knee and ,spine than in others = elbow , wrist and ankle. This is because some joints are more prone to predisposing factors than others.
Geographic distribution =very low incidence (virtual absence) of hip O.A in southern Chinese and African blacks , this is due to low incidence of predisposing factors e.g. DDH ,perthes disease in these populations.

8. 8 Risk factors = 1-joint dysplasia . 2-trauma .
3-occupation= repetitive stress .
4-bone density = negative association between O.A and osteoporosis.
5-obesity = positive association but this association is closer in women than in men so , it may reflect other endocrine or metabolic predisposing factors and not only the weight.
6-family history.

9. 9
Clinical features =
Patients usually present after middle age complaining of =
1- Pain = is the usual presenting symptom , it is often widespread or may be referred to a distant site e.g. pain of the knee from O.A of the hip .
2-Stiffness is common = it occurs after periods of inactivity , but with time it becomes constant and progressive.
3-Swelling may be intermittent (suggesting an effusion ) or continuous (with capsular thickening or large osteophytes ).
4-deformity = it may be the predisposing factor.
5-loss of function .
On examination = muscle wasting ,joint tenderness and sometimes synovial thickening or osteophytes can be felt.
Movement is always restricted but is often painless within the permitted range, and can be accompanied by crepitus.
In later stages muscle weakness and joint instability can occur.

10. 10
Imaging =
X- ray = in wt. Bearing joint should be in standing position.
1-decrease joint space.
2- subchondral cyst .
3-subchondral sclerosis.
4-osteophytes formation.
5-chondrocalcinosis may be found.
Arthroscopy =may show cartilage damage long before x-ray changes appear.

11. 11

12. 12 Complications of O.A = Management of O.A =
1-Capsular herniation= of posterior capsule (baker s cyst).
2-Loose bodies .
3-Rotator cuff dysfunction.
4-spinal stenosis.
5-spondylolisthesis.= due to facet joint O.A , especially L4 /L5.
Management of O.A =
1-Early stages =
Physiotherapy = muscle strength , massage , heat therapy , decrease wt. and analgesic medications.
2-Intermediate stages =
Joint debridement to wash pain mediators and loose bodies , and this can be done by arthroscope.

13. 13
Localized cartilage defects can be grafted with autologous chondrocytes.
Realignment osteotomy will act by =
-redistribution of loading forces towards less damaged parts of the joint.
-vascular decompression of the subchondral bone.
3-Late stages =
Arthrodesis = not widely used now.
Joint replacement arthroplasty.

15. 15

16. 16 Osteochondritis (osteochondrosis)=
This term is applied to a group of conditions in which there is compression , fragmentation ,or separation of a small segment of articular cartilage and bone.
This disorder occurs mainly in adolescents and young adults , often during phases of increased physical activity and may be initiated by trauma or repetitive stress.
1-Crushing osteochondritis =
It is characterized by apparently spontaneous necrosis of the ossific nucleus in a long bone epiphysis or one of the cuboidal bones of the wrist or foot.
Freiberg s disease of the metatarsal bones.
Kohler s disease of the navicular bone.
Kienbock s disease of the carpal lunate.
Panner s disease of the capitulum.

17. 17 Vertebral osteochondritis = Scheuermann s disease
2-Splitting osteochondritis ( osteochondritis dissecans)=
A small segment of articular cartilage and the subjacent bone may separate ( dissect ) as an avascular fragment.
E.g. - The lateral surface of the medial femoral condyle in the
knee.
-The antromedial corner of the talus in the ankle.
-The superomedial part of the femoral head.
-The humeral capitulum.
3-Pulling osteochondritis ( traction apophysitis ) =
Localized pain and increased radiographic density in an unfused apophysis may result from tensile stress on the physeal junction.
E.g. In tibial tuberosity = Osgood – schlatter s disease .
in calcaneal apophysis = Sever s disease.

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