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Osteoarthritis ppt


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Osteoarthritis ppt

  1. 1. Osteoarthritis (Degenerativearthritis/osteoarthrosis/hypertrophic arthritis)
  2. 2. Osteoarthritis Osteoarthritis is a non-inflammatory, degenerative condition of joints Characterized by degeneration of articular cartilage and formation of new bone i.e. osteophytes.
  3. 3.  Common in weight-bearing joints such as hip and knee. Also seen in spine and hands. Both male and females are affected. But more common in older women i.e. above 50 yrs,particularly in postmenopausal age.
  4. 4. Risk factors Obesity esp OA knee Abnormal mechanical loadingeg.meniscectomy, instability Inherited type II collagen defects inpremature polyarticular OA Inheritance in nodal OA Occupation eg farmers Infection:Non-gonococcal septic arthritisHereditary
  5. 5. Ageing process in joint cartilageDefective lubricating mechanismIncompletely treated congenitaldislocation of hip
  6. 6. Classification of OA OAPrimary OA Secondary OA
  7. 7. Primary OA More common than secondary OA Cause –Unknown Common-in elders where there is no previous pathology. Its mainly due to wear and tear changes occuring in old ages mainly in weight bearing joints.
  8. 8. Secondary OA Due to a predisposing cause such as:1.Injury to the joint2.Previous infection3.RA4.CDH5.Deformity6.Obesity7.hyperthyriodism
  9. 9. Types of OA Nodal Generalised OA • Crystal Associated OA • OA of Premature Onset
  10. 10. Nodal Generalised OA• • Heberden’s nodes• • Bouchard’s nodes• • CMC of thumb• • Hallux• valgus/rigidus• • Knees & hips• • Apophyseal joints
  11. 11. Crystal Associated OA• Calcium pyrophosphate• dihydrate occurs• mainly in elderly• women, and principally• affects the knee
  12. 12. OA of Premature Onset• • Previous meniscectomy• • Haemochromatosis
  13. 13. Pathology OA is a degenerative condition primarily affecting the articular cartilage.1.articular cartilage2.Bone3.Synovial membrane4.capsule5.Ligament6.muscle
  14. 14. Articular Cartilage Cartilage is the 1st structure to be affected. Erosion occurs,often central & frequently in wt. bearing areas. Fibrillation,which causes softening,splitting and fragmentation of the cartilage,occur in both wt. bearing & non-wt. bearing areas. Collagen fibres split and there is disorganisation of the proteoglycon collagen relationship such as H2O is attracted into cartilage, which causes futher softening and flaking.these flakes of cartilage break off and may be impacted b/w the jt.surfaces causing locking and inflammation.
  15. 15. Right: Early OA witharea of cartilage loss inthe center. Left: More advancedchanges with extensivecartilage loss andexposed underlyingbone
  16. 16. Arthroscopic appearancesin OA of the knee joint:fibrillated surface of thecartilage on the medialfemoral condyle
  17. 17. Bone(Eburnation) Bone surface become hard & polished as there is loss of protection from the cartilage. Cystic cavities form in the subchondral bone because eburnated bone is brittle and microfractures occur. Venous congestion in the subchondral bone.
  18. 18. Gross superior view of afemoral head from apatient with radiographicstage I OA. This shows anarea of complete cartilageloss, with polishing oreburnation of theunderlying bone.
  19. 19.  Osteophytes form at the margin of the articular surface,which may get projected into the jt. Or into capsule & ligament,bone of the wt.-bearing jt. There is alteration in the shape of the femoral head which becomes flat and mushroom shaped. Tibial condyles become flatened.
  20. 20. Osteophyte at margin of articular surface
  21. 21. Synovial Membrane Synovial membrane undergo hypertrophy and become oedematous (which can lead to ‘cold’ effusions). Reduction of synovial fluid secretion results in loss of nutrition and lubricating action of articular cartilage. CapsuleIt undergoes fibrous degeneration and there are low-grade chronic inflammatory changes
  22. 22. Ligament Undergoes fibrous degernation There is low grade chronic inflammatory changes and the aspect joint become contracted or elongated. MusclesUndergoes atrophy,as pt. is not able to use the jt. Because of pain which further limits movts. and function.
  23. 23. Clinical features of OA Pain Stiffness Muscle spasm Restricted movement Deformity Muscle weakness or wasting Joint enlargement and instability Crepitus • Joint Effusion
  24. 24. Clinical features 1• Pain and tenderness – Usually slow onset of discomfort, with gradual and intermittent increase – Pain is more on wt. bearing due to stress on the synovial membrane & later on due to bone surface,which r rich in nerve endings coming in contact. -initially relieved by rest but later on disturb sleep. -Diffuse/ sharp and stabbing local pain
  25. 25. Clinical features• Pain and tenderness (cont) – Types of pain • Mechanical: increases with use of the joint • Inflammatory phases • Rest pain later on in 50% • Night pain in 30% later on
  26. 26. Clinical features 2• Movement abnormalities – ‘Gelling’: stiffness after periods of inactivity, passes over within minutes (approx 15min.) of using joint again – Coarse crepitus: palpate/hear (due to flaked cartilage & eburnated bone ends) – Reduced ROM: capsular thickening and bony changes in joint,ms. Spasm or soft tissue contracture.
  27. 27. Clinical features 3• Deformities – Soft tissue swelling: • mild synovitis • small effusions – Osteophytes – Joint laxity – Asymmetrical joint destruction leading to angulation
  28. 28. Osteoarthritis of the DIPjoints. This patient hasthe typical clinicalfindings of advancedOA of the DIP joints,including large firmswellings (Heberden’snodes), some of whichare tender and red dueto associatedinflammation of theperiarticular tissues aswell as the joint.
  29. 29. Knee joint effusion
  30. 30. A patient withtypical OA of theknees. In the normalstanding posturethere is a mild varusangulation of theknee joints due tosymmetrical OA ofthe medialtibiofemoralcompartments.
  31. 31. Pseudolaxity due tocartilage loss. Thejoint is not loaded inthe first photograph
  32. 32. Unstable distalinterphalangealjoints in OA. Theexaminer is able topush the joint fromside to side due togross instability, acommon finding inlate interphalangealjoint OA.
  33. 33. Radiographic ClassificationStage 1 Bony spur onlyStage 2 Narrowing of jt. Space,less than half of the normal jt. spaceStage 3 Narrowing of jt. Space,more than half of the normal jt. spaceStage 4 Obliteration of jt. spaceStage 5 Subluxation or sec.lateral arthrosis
  34. 34. Distribution of OA of thehip joint. OA canmaximally affect thesuperior pole, inferiorpole, posterior part orother segments of thehip joint. Superior poleinvolvement, with atendency for the headof the femur to subluxsuperolaterally, is thecommonest pattern.Involvement of thewhole joint (concentricOA) is relativelyuncommon.
  35. 35. Special Investigations• Blood tests: Normal• Radiological features: – Cartilage loss – Subchondral sclerosis – Cysts – Osteophytes
  36. 36. Management
  37. 37. Treatment Principles• Education• Physiotherapy – Exercise program – Pain relief modalities• Aids and appliances• Medical Treatment• Surgical Treatment
  38. 38. Education• Nonsystemic nature of disease• Prevent overloading of joint. Obesity!!• Appropriate use of treatment modalities – Importance of exercise program – Aids, apliances, braces – Medial treatments – Surgical treatments
  39. 39. Exercise• Will not ‘wear the joint out’• Important for cartilage nutrition• Some evidence that lack of exercise leads to progression of OA
  40. 40. Exercise• Encourage full range low impact movements eg swimming, cycling• Avoid – Prolonged loading – Activities that cause pain – Contact sports – High impact sports eg running
  41. 41. Quadriceps exercisesfor knee OA.Quadriceps exercisesare of proven value forpain relief andimproving function, andeveryone with knee OAshould be taught thecorrect techniques andencouraged to makethese exercises alifetime habit. There is aweight on the ankle.
  42. 42. Use of transcutaneousnerve stimulation(TENS) as an adjunct toother therapy for painrelief at the knee joint.The use ofacupuncture, TENS andother local techniquesto aid pain relief indifficult cases of OA isoften worthwhile.
  43. 43. Aids and appliances• Braces / splints• Special shoes/insoles• Mobility aids• Aids: dressing, reaching, tap openers, kitchen aids• Taping of patella in patello femoral OA
  44. 44. Use of a cane, stick or other walking aid. This patient,who has hip OA, has found that she can reduce thepain in her damaged left hip by leaning on the stick inthe right hand as she walks. The reduction in loadingcan be huge, and the effect on symptoms andconfidence with walking very beneficial.
  45. 45. The use of shoes andinsoles to reduceimpact loading on lowerlimb joints. Modernsports shoes (‘trainers’)often have appropriateinsoles. Alternatively,special heel or shoeinsoles of sorbithane orviscoelastic materialscan be used. They mayhelp relieve pain as wellas reducing the peakimpact load on thejoints during walking.
  46. 46. Medical Treatment• Simple analgesics: paracetamol, low dose ibuprofen• NSAID’s/Coxibs PRN regular• Intra-articular corticosteroids• Topical treatment eg NSAID creams, capsaicin• ‘Chondroprotective agents’
  47. 47. A patient with OA of thecarpometacarpal joint ofthe left thumbundergoingarthrocentesis forinjection of a depotcorticosteroidpreparation. Theoperator is distractingthe patient’s thumb toopen up the joint space.
  48. 48. Joint replacement surgery• Indications: pain affecting work, sleep, walking and leisure activities• Complications – sepsis – loosening – lifespan of materials (mechanical failure)