Osteoarthritis lecture for UG


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Osteoarthritis lecture for UG

  1. 1. OSTEOARTHRITIS Dr Dhananjaya Sabat MS, DNB, MNAMS Assistant Professor MAMC & STC
  2. 2. A chronic joint disorder in which there isprogressive softening and disintegrationof articular cartilage accompanied by newgrowth of cartilage and bone at the jointmargins (osteophytes) and capsularfibrosis
  3. 3. OA Classification Trauma Primary or Osteonecrosis idiopathic: MC Inflammatory Arthritis, Pseudogout, joint knee Ochronosis, Wilsons disease, Hemochromatosis Septic arthritis Secondary: SCFE, DDH, Skeletal dysplasia Secondary to Ehler Danlos syndrome, Marfan some preexisting syndrome abnormality Acromegaly, Hyperparathyroidism Recurrent hemarthrosis (hemophillia) Kashin-Beck disease Neuropathic (Charcot’s)
  4. 4. OA Etiology Genetic Metabolic Hormonal Mechanical Ageing
  5. 5.  Location- most common joint involved are knee and hip OA of DIP joint leads to “Herberdens nodes”. It has genetic predisposition. Nodes on PIP joints are called" Bouchards nodes"
  6. 6. OA MechanismDisparity between:-stress applied to articular cartilage & strength of articular cartilage increased load e.g. BW or Weak cartilage activity  age decreased area e.g. varus  stiff e.g. ochronosis knee or dysplastic hip  soft e.g. inflammation  abnormal bony support e.g. AVN
  7. 7. OA Pathology OA is a gradual process of destruction & regeneration Early in disease, articular cartilage loses its glistening appearance Later on surface layers flake off while deeper layers develop longitudinal fissures, process termed fibrillation Cartilage becomes thin and sometimes denuded CARTILAGE EROSION CARTILAGE ULCERATION
  8. 8.  Subchondral bone: Becomes thickened, sclerotic, & polished (eburnation) Subchondral bone displays thickened trabeculae and microfractures Tidemark is disrupted by vessels from the subchondral layer Cysts: May be seen in subchondral bone Cysts may arises from increases in intrasynovial pressure
  9. 9.  Osteophytes: Spur like bony outgrowths covered by hyaline cartilage, may develop at margins of joint & progressively enlarge Small bits of cartilage-covered bone, known as joint mice, may actually break off into the joint
  10. 10. OA Knee grading
  11. 11. Normal Cartilage
  12. 12. OA Histology Articular cartilage: Superficial zone demonstrates earliest changes; Diminution of chondrocytes. Cartilage matrix loses its ability to stain for proteoglycans with alcian blue or safranin-O. Deeper chondrocytes - proliferation in clusters (brood capsules) Capillary buds penetrate the layer of calcified cartilage Newly formed sements of cartilage push up from below Tidemark: Demarcation between calcified and noncalcified cartilage; Becomes split & reduplicating tidemark
  13. 13.  Synovium: becomes hypertrophied and thrown into villous folds; May see infiltration with plasma cells, and lymphocytes; Synovial hypertrophy may be involved in producing joint pain by increased synovial fluid production and increased intra- articular pressure.
  14. 14. OA Cytokines
  15. 15. FAI Femoroacetabular impingement hip clearance secondary to poor orientation/depth of acetabulum shape of head-neck junction Two types: Cam & Pincer Precurser to OA hipEtiology• Acetabular retroversion• Protrusio, coxa profunda• Non-spherical head, Perthes, out of round head• SCFE• femoral offset (poor head-neck ratio)• Retroverted femoral neck post fracture
  16. 16. CROSSOVER SIGNEvaluation of FAI
  17. 17. OA X-ray changes Joint space narrowing Subchondral sclerosis Osteophytes Subchondral cysts
  18. 18. OA Symptoms Pain Crepitus Swelling / effusion Stiffness Deformity Instability Loss of functionDeformity: In Knee: Genu Varum (valgum in c/o RA) In Hip: flexion, trendelenburg gait
  19. 19. OA Management
  20. 20. OA Core treatment Altered activity Exercise and manual therapy irrespective of age, comorbidity, pain severity or disability. Exercise should include: local muscle strengthening, and general aerobic fitness. Manipulation and stretching should be considered as an adjunct; esp. in OA hip. Reduction of cartilage impact loading: (typically this is 6 times body wt)- Cane (opposite hand) Rubber heel wedges (consider lateral wedges for medial compartment arthrosis) Wt loss: for overweight pts Braces Thermotherapy local heat or cold as an adjunct. Electrotherapy TENS as an adjunct.
  21. 21. OA Drug T/T Paracetamol : 1st line analgesic, upto 1gm/6hrly Topical NSAID, Topical capsaicin should be considered as an adjunct If paracetamol or topical NSAIDs are insufficient for pain relief for people with osteoarthritis, then the addition of opioid analgesics should be considered. No oral NSAID, COX-2 inh. . If reqd., with PPI.
  22. 22.  Nutraceuticals The use of glucosamine or chondroitin products is not recommended Disease modifying drugs (RA): Diacerine S-Adenosyl Methionine: lack of clinical evidence. Intra-articular corticosteroid as an adjunct for the relief of moderate to severe pain. 40mg Triamcinalone (1ml) with 4ml Lidocaine. Not to be repeated in 3mo. Intra-articular hyaluronan (Synvisc, Hyalgan) are used for temporary pain relief, 60-70% pts get benefit upto 6mo; not recommended as per NICE guidelines.
  23. 23. OA Invasive treatmentKnee- Arthroscopic lavage and Arthrodesis rarely indicated - debridement in small joints of hand, HTO (High tibial osteotomy) wrist and ankle. Joint replacement : Excission arthroplasty is Unicondylar, Patellofemoral, TKR rarely indicated – 1st CMC joint.Hip- Valgus extension osteotomy Surface replacement THR
  24. 24. OA Evaluation Pain EXAMINATION Gait Function:  Walking distance  Limb alignment walking aids  Range of movement low chairs  Stability foot care  Peripheral circulation Stairs Skin condition  Medical Expectations
  25. 25. OA Investigation X-ray - Alignment - Deformity - Previous fractures and implants - AVN - Osteophytes - Bone loss CT, MRI, bone scan - rarely
  26. 26. Arthroscopic debridement Joint fluid washout Removal of loose cartilage Ostyophytectomy Synovectomy Effective in early stage disease May be combined with HTO
  27. 27. High tibial osteotomy Realignment of knee wt bearing axis to transfer load from medial to lateral compartment Effective for 5-10yrs ACL/PCL deficiency can be addressed. OPEN WEDGEIndications: Unicompartmental arthritis Age <60yrs Genu varus / valgus < 15 deg flexion deformity ROM > 90 deg No lateral thrust CLOSED WEDGE
  28. 28. Unicompartmental kneereplacementIndications Unicompartmental arthritis Low-demand patients who are older than 60 Weight less than 82 kg Minimum 90° flexion arc Flexion contracture of less than 5° Angular deformity not exceeding 10° of varus or 15° of valgus (both of which should be correctable to neutral passively after removal of osteophytes), Intact anterior cruciate ligament (ACL) No pain or exposed bone in the patellofemoral or opposite tibiofemoral compartment.
  29. 29. Patellofemoral replacement For isolated patellofemoral arthritis
  30. 30. Total knee replacement For advanced tricompartmental arthritis