OSTEOARTHRITIS

Dr Dhananjaya Sabat MS, DNB, MNAMSAssistant Professor

MAMC & STC

A chronic joint disorder in which

there is progressive softening and disintegration of articular cartilage accompanied by new growth of cartilage and bone at the joint margins (osteophytes) and capsular fibrosis

OA Classification

Primary or idiopathic: MC joint knee

Secondary: Secondary to some preexisting abnormality

TraumaOsteonecrosis Inflammatory Arthritis, Pseudogout, Ochronosis, Wilson's disease, HemochromatosisSeptic arthritis SCFE, DDH, Skeletal dysplasiaEhler Danlos syndrome, Marfan syndromeAcromegaly, 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 “Herberden's nodes”. It has genetic predisposition.

Nodes on PIP joints are called" Bouchard's nodes"

OA Mechanism

Disparity between:- stress applied to articular cartilage & strength of articular

cartilageWeak cartilage age stiff e.g.

ochronosis soft e.g.

inflammation abnormal bony

support e.g. AVN

increased load e.g. BW or activity

decreased area e.g. varus knee or dysplastic hip

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 denudedCARTILAGE 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

Normal Cartilage

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.

OA Cytokines

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

Evaluation of FAICROSSOVER SIGN

OA X-ray changes

Joint space narrowing

Subchondral sclerosis

Osteophytes Subchondral cysts

OA Symptoms Pain Crepitus Swelling / effusion Stiffness Deformity Instability Loss of function

Deformity: In Knee: Genu Varum (valgum in c/o RA) In Hip: flexion, trendelenburg gait

OA Management

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 treatment

Knee- Arthroscopic lavage and

debridement HTO (High tibial osteotomy) Joint replacement :

Unicondylar, Patellofemoral, TKR

Hip- Valgus extension osteotomy Surface replacement THR

Arthrodesis rarely indicated - in small joints of hand, wrist and ankle.

Excission arthroplasty is rarely indicated – 1st CMC joint.

OA Evaluation

Pain Function: Walking distance walking aids low chairs foot care Stairs

Medical Expectations

EXAMINATION Gait Limb alignment Range of movement Stability Peripheral circulation Skin condition

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.

Indications: Unicompartmental arthritis Age <60yrs Genu varus / valgus < 15 deg flexion deformity ROM > 90 deg No lateral thrust

OPEN WEDGE

CLOSED WEDGE

Unicompartmental knee replacementIndications 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 REPLACEMENT

TOTAL HIP REPLACEMENT