Osteoarthritis is a chronic joint disorder involving the progressive breakdown of articular cartilage and changes in the underlying bone. It most commonly affects the knees and hips. Risk factors include age, genetics, previous joint injury, and excessive weight. Symptoms include pain, stiffness, swelling, and loss of function. Treatment focuses on reducing pain and inflammation, maintaining joint mobility, managing weight, and modifying activities. Surgery such as joint replacement may be considered if more conservative measures fail to provide adequate relief.

1. OSTEOARTHRITIS
Dr Dhananjaya Sabat MS, DNB, MNAMS
Assistant Professor
MAMC & STC

2. 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

3. OA Classification
Trauma
 Primary or Osteonecrosis
idiopathic: MC Inflammatory Arthritis, Pseudogout,
joint knee Ochronosis, Wilson's 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. OA Etiology
 Genetic
 Metabolic
 Hormonal
 Mechanical
 Ageing

5.  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"

6. OA Mechanism
Disparity 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. 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.  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.  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

11. OA Knee grading

12. Normal Cartilage

13. 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

14.  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.

15. OA Cytokines

16. FAI Femoroacetabular impingement
 hip clearance secondary to poor orientation/depth of
acetabulum shape of head-neck junction
 Two types: Cam & Pincer
 Precurser to OA hip
Etiology
• 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

18. CROSSOVER SIGN
Evaluation of FAI

19. OA X-ray changes
 Joint space narrowing
 Subchondral sclerosis
 Osteophytes
 Subchondral cysts

22. 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

23. OA Management

24. 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.

25. 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.

26.  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.

27. OA Invasive treatment
Knee-
 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

28. 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

29. OA Investigation
 X-ray - Alignment
- Deformity
- Previous fractures and implants
- AVN
- Osteophytes
- Bone loss
 CT, MRI, bone scan - rarely

30. Arthroscopic debridement
 Joint fluid washout
 Removal of loose
cartilage
 Ostyophytectomy
 Synovectomy
 Effective in early stage
disease
 May be combined with
HTO

31. 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

32. Unicompartmental knee
replacement
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.

33. Patellofemoral replacement
 For isolated patellofemoral arthritis

34. Total knee replacement
 For advanced tricompartmental arthritis

35. Replacement of hip
SURFACE TOTAL HIP
REPLACEMENT REPLACEMENT