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

2. 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

3. 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)

4. Articular Cartilage

5. 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

6. Articular Cartilage

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

8. 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

9. 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

10. 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

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

15. Classification

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

17. Joints involved
Hands: DIP, 1st CMC
Knees
Spine

18. Secondary OA
Increase load
Abnormal cartilage
Abnormal support

19. Increase Load, overweight

20. Increase Load, deformity

21. Increase Load, occupation

22. Increase Load, joint incongruity

23. Increase Load, athletes

24. Diseased Cartilage, infection

25. Diseased Cartilage, crystal deposition

26. Diseased Cartilage, inflammatory arthritis

27. Abnormal Support, AVN

28. Abnormal Support, intra-articular fractures

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

31. Examination Deformity Swelling Tenderness Crepitus Range of movement
Signs of inflamation

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