OSTEOARTHRITIS

Dr Dhananjaya Sabat MS, DNB, MNAMS

Assistant 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

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
Acromegaly, Hyperparathyroidism
abnormality

Recurrent hemarthrosis (hemophillia)

Kashin-Beck disease
Neuropathic (Charcots)

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 cartilage

increased load e.g. BW or

activity
decreased area e.g. varus
knee or dysplastic hip

Weak cartilage

age

stiff e.g. ochronosis

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

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 intraarticular 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 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

Evaluation of FAI

CROSSOVER 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:

EXAMINATION

Walking distance
walking aids
low chairs
foot care
Stairs

Medical
Expectations

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:

OPEN WEDGE

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

CLOSED WEDGE

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.

Patellofemoral replacement
For isolated patellofemoral arthritis

Total knee replacement

For advanced tricompartmental arthritis

Replacement of hip

SURFACE
REPLACEMENT

TOTAL HIP
REPLACEMENT