Osteoarthritis is a chronic disorder of synovial joints characterized by progressive cartilage destruction, subarticular bone changes like cyst formation and sclerosis, and osteophyte formation. It results from an imbalance between cartilage breakdown and repair. Risk factors include joint injury, obesity, genetics, and age. Symptoms include joint pain, stiffness, swelling and loss of function. Imaging shows characteristic changes and management focuses on maintaining joint mobility, reducing pain and considering surgery for late stages.

1. OSTEOARTHRITIS

2. The physiology of synovial joints
• Diarthrodeal joint is covered with hyaline
cartilage.
• Covers subarticular bone
• Covered by synovial fluid-slippery and offer very
little friction resistance to mvt &surface gliding.
• Chrondrocytes af adult cartilage have very little
capacity for cell division.
• damage to the articular surface is poorly repaired
with fibrocartilage

3. • Proteoglycan-chondroitin sulphate, keratan
sulphate.
• Threats to cartilage integrity
– Loss of joint stability
– Localized increase in loading stress
– Increased stiffness of the cartilage
– Inflammatory (enzymatic) degradation
– Restriction of free jt mvt
– Schlerosis of subchondral bone

4. Capsule and ligaments
• Made of dense fibrous tx with the overlying muscles help to
provide stability
• SYNOVIUM &SYNOVIAL FLUID
• The anterior surface of the capsule is lined by a thin
membrane(synovium)-richly supplied with blood vesssels,
lymphatics and nerves
• Provides a non adherent covering of the srticular surface &
produce synovial fluid
• The fluid nourishes the avascular articular cartilage, reduce
friction &has adhesive properties
• In normal life, the volume of synovial fluid remain constant

5. • Increase when jt is injured- jt effusion or infxn, &
autoimmune disorders e.g r.a
• Jt lubrication;
1. Boundary layer lubrication-single layer water,
soluble glycoprotein, lubricin.
2. Fluid film lubrication
3. Lubrication btn synovial folds is protected by
hyaluronate.

6. osteoarthritis
• A chronic disorder of synovial joints
• There is progressive softening and
disintegration of articular cartilage
accompanied by new growth of cartilage and
bones at the jt margins (osteophytes) cyst
formation & schlerosis of the subchondral
bone, mild synovitis & capsular fibrosis.

7. • In its most common cause, it is not
accompanied by any systemic illness & it is not
an inflammatory disorder.
• Though it is assd with local signs of
inflammation
• It is not purely a degenerative disorder
• It is a dynamic disorder- show both features of
destruction and repair

8. • Cartilage destruction (softening &
disintegration)+ hyperactive new bone
formation, osteophytosis and remodelling
• Secondary factors:
– Calcium containing crystals in the jt
– Ischaemic changes
– Effect of prolonged anti-inflammatory medicines

9. etiology
• Increases in frequency with age
• Cartilage ages: this predisposeto O.A
• Primary changes in cartilage matrix might
weaken its structure & predispose to cartilage
breakdown- crystal deposition dx &
onchronosis
• Inheritance- increase in first degree relatives
• Primary deformity at molecular level

10. • Articular cartilage may be damaged by trauma
or previous inflammatory disorder
• Enzymes released by synovial cells &
leukocytes can cause leaching of
proteoglycans from the matrix & synovial
derived IL1 may suppress proteoglycan
synthesis cause secondary o.a in R.A dx

11. Primary idiopathic o.a
• Precipitating cause is increase in mechanical
stress in some part of the articular surface.
• Due to increased load or deformities or
reduction of articular contact area eg varus
deformity of knee or acetabular dysplasia
• Changes in subchondral bone may alter the
shape of articular cartilage.
• Primary- there is no obvious antecedent factor
• Secondary- follow demonstrable abnormality

12. pathogenesis
• Early changes; increase in water content of
cartilage and easier extractability of matrix
proteoglycans
• Later there is loss of proteoglycans & defects
appear in the cartilage
• As cartilage become less stiff; secondary damage
to chondrocytes may cause release of cell
enzymes & further matrix breakdown
• The cartilage serves to distribute forces & when
lost , these forces are increasing concentrated to
subchondral bone

13. • Result; focal trabecular degeneration & cyst
formation as well as increased vascularity &
reactive schlerosis in the zone of maximal
loading
• The joint surfaces become inceasingly
malopposed & jt unstable, cartilage at the
edge of the jt give rise to osteophytes

14. PATHOLOGY
• CARDINAL FEATURES;
– Progressive cartilage destruction
– Subarticular cyst formation
– Schlerosis of surounding bone
– Osteophytes
– Capsular fibrosis
• Initially cartilage and bony changes are confined
to one part of the jt- the most heavily loaded
• Chondromalacia

15. • With progressive degeneration of cartilage,
the underlying bone become exposed & some
areas may be polished, or burnished to ivory
like smoothness(eburnation)
• Ends of joints grow osteophytes
• Beneath the damaged cartilage the bone is
thick & schlerotic (subchondral schlerosis) or
small cyst

16. prevalence
• Comonest of all jt dxs
• Men & women equally affected
• More jts are affected in women
• More common in fingers, hip, knee &spine
than in others, elbow wrist & ankle.
• Modified by geographic and ethnic
differences.
• Predisposing disorders; ddh, perthes, sufe

17. Risk factors
• Joint dysplasia-congenital acetabular dysplasia, perthes
dx
• Trauma-secondary osteoarthritis/injury result injt
instability
• Occupation-causing repetitive stress/ upper limbs if
working with heavy vibrating tools/ cotton mill workers
• Sports-boxer-hands, football-knee, baseball pitchers-
shoulder
• Bone density- BMDincrese
• Obesity-INCREASE joint loading
• Family hx-women whose mothers had o.a

18. symptoms
• Pt usually present after middle age
• Jt involvement follow different patterns
• Pain; referred pain/
• Stiffness
• Swelling-intermittent (effusion)/continuous
capsular thickening or large osteophytes
• deformity
• Loss of fxn
• Deformity
• Loss of function

19. Signs
• Jt swelling
• Tell tale scar
• Muscle wasting
• Deformity
• Local tenderness
• Limited mvt
• Crepitus
• Instability
• Other jts

20. IMAGING
• X-ray; xtic appearance
• Radionuclide scanning
• Ct scan &mri
• arthroscopy

21. complications
• Capsular herniation( bakers cyst)
• Loose bodies
• Roatator cuff syndrome
• Spinal stenosis
• spondylolithesis

22. mgt
• Depend on jts involved
• The stage of the disorder
• The severity of symptoms
• The age of the pt / functional needs

23. early
• There is as yet no drug that can modify the
effects of oa
• Rx is symptomatic
• Principles
– Maintain mvt & muscle strength
– Protect the jt from overload
– Relieve pain
– Modify daily activities

24. • Physical therapy
• Load reduction
• Analgesics
• Intermediate
– Jt debridement
– Remove loose bodies
• Late
– Reconstructive sx
– 3 types
– Realignment
– Arthroplasty
– arthrodesis