osteoarthritis Flashcards
Define osteoarthritis
Commonest form of arthritis – present in most people over 60 to some extent.
‘Wear + Tear’ or ‘Degenerative Joint Disease’
Pathology of osteoarthritis
Loss of cartilage, narrowing of the joint space, low grade synovial inflammation, thickening of subchondral bone and development of bony outgrowths - osteophytes
Features of OA
abnormal loading of normal tissues/normal loading of abnormal issues gives progressive OA
ability of tissues to adapt and respond to injury and insult/ repair potential gives stabilisation or repair
Risk factors for OA
age - time to develop and respond to injuries - old cartilage repairs less well , reduced muscle strength and bulk and reduced joint propioception w age
systemic factors (genetic/environment) - twins show 65% concordance of OA ; multiplicity of genes involved-complex
local biochemical factors
obesity 30-35 BMI x4 increased risk of knee OA
sex- women have more knee(mechanical) and hand(Endocrine) OA
trauma/injury
joint shape
repetitive use
muscle weakness
joint laxity
occupational factors
determine site and severity of OA
Symptoms/Signs of OA
Pain and stiffness
Gel phenomenon, stiffness after immobility
Worse with prolonged use
Poor correlation with radiographs
Multiple factors influence pain including cognitive, emotional, stress, sleep etc.
signs; heberdens, bouchards nodes, genu varus
Patterns of OA
Hands and Feet (Heberden’s , Bouchard’s nodes, Generalised OA)
Spine
Large weight bearing joints
Generalised or just a few joints
Typical patterns but most joint can be affected
Pathophysiology of osteoarthritis
-wear and tear of cartilage
- chondrocytes in early OA- metabolically active + help repair but as OA progresses, chondrocytes get distressed and Cytokines TNF-a, IL-1, IL-6, collagenases, metalloprotineases, aggrecanases – are released from inflam cells & important in degradation
causes chondrocyte apoptosis, loss of proteoglycans and collagen fibril damage and bone sclerosis
IL4, TGFb, IGF1, TIMP - protective cytokines
How do you view cartilage?
via arthroscope
Diagnosis of OA
CLINICAL Often History and exam is enough- typical patterns of symptoms and joints involved
Blood tests normal (unlike RA)- mostly to R/O other types arthritis
Xrays late on show joint space narrowing, osteophytes, sclerosis
What are the goals of OA
Relieve pain
Maintain or restore function with rehabilitation and exercise
Delay progression if possible
Pharm tx for pain
Paracetamol should be tried first - many will respond
NSAIDs & Coxibs should be tried next – many (but not all) patients will respond better- ibruprofen, diclofenac,naproxen - inhibits prostaglandin production
Mild opiates – co-proxamol, codeine, Tramadol
Start with the simplest and use as needed for symptom management only
Side effects of NSAIDS
gastritis, GI bleeds
can aggrevate renal impairment and hypertension
increase CV risk w pts with ischaemic heart disease
coxibs are GI safe
Physical management of pain
Use of Heat & Cold - hot packs, hot water, cold pack provide symptomatic relief
Evidence for other physiotherapy Tx is weak but it may provide some relief
Acupuncture – few good trials
Other pharm tx?
IA hyaluronic acid derivatives may have a trophic effect on cartilage – given in a course of 3-4 IA injections
Intra-articular depot corticosteroids - give effective but short term relief
Other aspects of OA to be treated?
depression - tx needed; promotion of self efficacy
diet
exercise