Osteoarthritis lecture for UGPresentation Transcript
OSTEOARTHRITIS Dr Dhananjaya Sabat MS, DNB, MNAMS Assistant Professor MAMC & STC
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
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)
OA Etiology Genetic Metabolic Hormonal Mechanical Ageing
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"
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
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
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
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
OA Knee grading
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
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.
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
CROSSOVER SIGNEvaluation of FAI
OA X-ray changes Joint space narrowing Subchondral sclerosis Osteophytes Subchondral cysts
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
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.
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.
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.
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
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
OA Investigation X-ray - Alignment - Deformity - Previous fractures and implants - AVN - Osteophytes - Bone loss CT, MRI, bone scan - rarely
Arthroscopic debridement Joint fluid washout Removal of loose cartilage Ostyophytectomy Synovectomy Effective in early stage disease May be combined with HTO
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 WEDGEIndications: Unicompartmental arthritis Age <60yrs Genu varus / valgus < 15 deg flexion deformity ROM > 90 deg No lateral thrust CLOSED WEDGE
Unicompartmental kneereplacementIndications 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.
Patellofemoral replacement For isolated patellofemoral arthritis
Total knee replacement For advanced tricompartmental arthritis
Replacement of hip SURFACE TOTAL HIP REPLACEMENT REPLACEMENT