OSTEOARTHRITIS DR. WALEED HADDAD CONSULTANT ORTHOPAEDICS HAND & UPPER LIMB SURGEON ASS. PROF./FACULTY OF MEDICINE/BALQA APPLIED SCIENCE UNIVERSITY

Introduction Most common joints condition Affects daily activity  morbidity and financial burden Weight bearing joints affected more than non weight bearing strongly related to age

Epidemiology After age of 60, 10 to 15% has symptoms of OA Female more than males and more generalized disease Women have more hand OA (PIP, DIP) Racial variation Caucasian = African American but African American more sever Chinese have less hip OA and more Knee OA (arabs)

Articular Cartilage

Hyaline Cartilage, Composition Chondrocyte occupy lacunae generously distributed through the matrix approx 10% of wet weight of cartilage is collagen Mainly type II Little of IX and XI approx 75% of matrix is water remainder is a nonfibrous filler material Glycoseaminoglycane: chondroitin and keratin sulfate these entities together form stiff structure

Articular Cartilage

Function of Articular Cartilage Gliding surface Shock absorbent: compressed by 40% Weight distribution

Pathophysiology of OA Cartilage Osteoarthritis represents a gradual processes of destruction & regeneration Early in dz, 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 Collagen fiber structure is altered and the number and quality of proteoglycan aggregates decreases Chondrocytes releases more and more PGE2 Prostaglandin-stimulated release of matrix metalloproteinases: may lead to cartilage degradation

subchondral bone: cysts: 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: Synovium: spurlike 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 Synovium: becomes hypertrophied and thrown into villose folds may see infiltration with plasma cells, and lymphocytes syovial hypertrophy may be involved in producing joint pain by increased synovial fluid production and increased intra-articular pressure

Capsule Ligaments Areas of fibrosis which leads to contractures Laxity leads to deformities

Classification

Primary OA Age Sex: more in females Primary OA > 40 years Direct correlation Aging process Sex: more in females

Joints involved Hands: DIP, 1st CMC Knees Spine

Secondary OA Increase load Abnormal cartilage Abnormal support

Increase Load, overweight

Increase Load, deformity

Increase Load, occupation

Increase Load, joint incongruity

Increase Load, athletes

Diseased Cartilage, infection

Diseased Cartilage, crystal deposition

Diseased Cartilage, inflammatory arthritis

Abnormal Support, AVN

Abnormal Support, intra-articular fractures

Presentation Pain (site, duration, ….) Stiffness: typically less than 30 minutes Swelling: bony or effusion Deformity: primary or secondary Weakness: due to pain

Examination Deformity Swelling Tenderness Crepitus Range of movement Signs of inflamation

Treatment From simple analgesia    surgery Debridement Osteotomy Joint replacement arthrodesis