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
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
