Osteoarthritis is a chronic joint disorder characterized by the progressive breakdown of articular cartilage. It is not primarily inflammatory but rather a dynamic process of destruction and repair. Risk factors include aging, genetics, previous joint injuries or inflammation, and mechanical stress from factors like deformity or instability. Clinically, patients experience pain, stiffness, swelling and deformity of the joint. Imaging shows decreased joint space, bone spurs, and other signs of cartilage damage. Treatment focuses on managing symptoms via medications, physical therapy, bracing, and sometimes surgery.

1. OSTEOARTHRITIS
Lecture 1
Dr. Hussein M.
Azeez

2. ANATOMY AND PHYSIOLOGY
OF THE SYNOVIAL JOINT

6. OSTEOARTHRITIS
DEFINITION
OF OA
Is a chronic joint disorder in which there is progressive
softening and disinteg-ration of articular cartilage accompanied
by new growth of cartilage and bone at the joint margins and
capsular fibrosis.
Articular cartilage has matrix which
consists of proteoglycan ground
substance that contains collagen
(type II) network and chondrocytes.
It has compressibility and elasticity
to make the joints’ movements
easier.
Fibrilation of the articular cartilage
after trauma or inflammation will
occur.

7. DEFINITION
CONT.
Although there are sometimes local signs of inflammation, it is
not primarily an inflammatory disorder.
It is not purely degenerative disorder; although , degenerative
arthritis some-times used for osteoarthritis.
It is dynamic process (destruction and repair).
Age: aging of the cartilage
shows:
Diminished cellularity.
Reduced proteoglycan
concentration.
Loss of elasticity.
Decrease in breaking
Note: these changes are
restricted to certain joints and
to specific areas of these
joints, while other areas
shows little or no progression
with age.
Note2: deformities and
fractures can initiate OA in an
ETIOL
OGY

8. ETIOLOGY
CONT.
Primary changes in cartilage matrix: like in crystal
deposition diseases and genetic defects in type II collagen.
Previous inflammatory disorders: this might causes
articular cartilage damage and the enzymes that released by
synovial cells and leucocytes can affect proteoglycans. E.g.
secondary OA can occur in patients with rheumatoid arthritis.
Increased mechanical stress with joint overloading is
the major factor and this can be due to:
Increased load; in deformity and instability.
Changes in the subchondral bone; can change the shape of the
articular cartilage or can reduce the shock absorbing effect of
the supporting cancellous bone by increasing bone density.

10. PATHOGE
NESIS
1. 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.
2. At slightly later stages there is loss of proteoglycans and
defects appear in the cartilage.
3. As the cartilage becomes less stiff, secondary damage to
chondrocytes may cause release of cell enzymes and further
matrix breakdown.
4. When the articular cartilage loses it’s integrity, there will be
more force on the subchondral bone and so there will be
trabecular degeneration and cyst formation.
5. There will be increased vascularity and reactive sclerosis in
the zone of maximal loading.
Note: cartilage at the edges of the joint still has the activities
of growth and enchondral ossification giving rise to
osteophytes.

15. Figure 5.5
Osteoarthritis –
histology
(a) Destructive
changes (loss of
articular cartilage
and cyst formation)
are most marked
where stress is
greatest; reparative
changes are
represented by
sclerosis around the
cysts and new bone
formation
(osteophytes) in less
stressed areas.
(b) In this high-power view,
the articular cartilage
shows loss of
metachromasia and deep
clefts in the surface
(fibrillation). Attempts at
repair results in
(c) subarticular sclerosis
and buds of fibrocartilage
mushrooming where the
articular surface is

16. PREVAL
ENCE
It is the commonest disease among all the joint diseases.
Autopsy studies show OA changes in everyone over the age of
65 years.
Men and woman are equally affected, but more joints affected
in woman than in men.
OA 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 (virtually absence)
of hip OA in southern Chinese and African blacks, this is related
to the low incidence of predisposing factors e.g. DDH and
Perthe’s disease in these populations.

17. CLINICAL
FEATURES
Patients usually in the middle age complaining from:
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 OA 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 and activities: limping, difficult
handling and handwriting, ..etc.

18. O/E: muscle wasting, joint tenderness and sometimes
synovial thickening or osteophytes can be felt. Crepitus on
movement of the joint.

19. 5.8 Osteoarthritis – x-rays The cardinal features of osteoarthritis are remarkably
constant whether in a) the hip, (b) the knee or (c) the ankle: loss of articular
cartilage seen (as narrowing of the ‘joint space’,
subarticular
cyst formation
and sclerosis,
osteophyte
formation and
bone
remodelling.

20. IMAGI
NG
X-ray: in weight bearing
joint should be in standing
position. It will show:
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.
COMPLICAT
IONS
1. Capsular herniation of
posterior capsule (Baker’s
cyst).
2. Loose bodies.
3. Rotator cuff dysfunction.
4. Spinal stenosis.
5. Spondylolisthesis: due to
facet joints OA, especially
L4/L5 facet joint.

22. MANAGEM
ENT

23. NEUROPATHIC JOINT
DISEASE
(CHARCOT'S DISEASE)
Definition:
Destructive arthropathy arising
from loss of pain sensibility and
position sense.
Most common causes:
Diabetes Melitus
Syringomylia,
Multiple sclerosis
Peripherial neuritis(diabetes
mellitus)
Leprosy
Neurosyphlis

24. Clinical Features
1. Weakness, instability ,swelling and laxity.
2. Progressive deformity of the joint.
3. Sensation that the joint neither warm nor particularly tender.
4. The paradox is diagnostic There is always some instability
and in the worst cases the joint is flail. The appearances
suggest that movement would be agonizing and yet it is
often painless. The paradox is diagnostic. General
examination may reveal features of the underlying
neurological disorder.

25. X-ray
The radiogaphic changes may at first be mistaken for those of
osteoarthritis.
However, thinning of the articular space is unusually rapid
Little osteophyte formation.
Joint swelling and the appearance of intra-articular
‘calcification’ are further clues.
Ultimately there is gross erosion of the articular surfaces and
displacement of the joint.

26. Treatment
There is no way of halting or slowing the destructive
process
Usually conservative consist of splintage of unstable
joint, despite the bizarre appearance patients seems
to manage well.
Arthrodesis may be attempted, but the patient
should be warned that there is only a small chance of
success.