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OSTEOARTHRITIS

Osteoarthritis (OA) is a prevalent chronic joint disorder characterized by cartilage degradation and subchondral bone repair, influenced by mechanical, biochemical, and genetic factors. It primarily affects older adults, particularly women, and leads to significant pain, disability, and economic burden. Management involves a multidisciplinary approach focusing on education, pain relief, and functional optimization, utilizing both non-pharmacological and pharmacological treatments.

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Ehis Hamilton
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0% found this document useful (0 votes)
27 views39 pages

OSTEOARTHRITIS

Osteoarthritis (OA) is a prevalent chronic joint disorder characterized by cartilage degradation and subchondral bone repair, influenced by mechanical, biochemical, and genetic factors. It primarily affects older adults, particularly women, and leads to significant pain, disability, and economic burden. Management involves a multidisciplinary approach focusing on education, pain relief, and functional optimization, utilizing both non-pharmacological and pharmacological treatments.

Uploaded by

Ehis Hamilton
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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OSTEOARTHRITIS

400L STUDENTS LECTURE SERIES

DR AIRENAKHO EMORINKEN MBBS, FMCP


OUTLINE
• Introduction
• Anatomy of the joint
• Epidemiology
• Classification/types
• Pathophysiology
• Presentation
• Investigations
• Treatment
• Take Home
INTRODUCTION
• Osteoarthritis (OA) is a complex, active degradative and repair
process of cartilage and subchondral bone, with a synovial
inflammation

• Mechanical stress, biochemical and genetic factors play a role

• Chondrocytes respond to injuries by producing degradative enzymes


and by developing inappropriate repair responses
• It is the most common chronic joint disorder, resulting in pain and
deformity, ultimately leading to chronic disability.

• Hence, it’s rapidly becoming a significant medical and financial burden


in a world whose population is ageing (except probably in Nigeria).

• Optimal management requires early diagnosis and awareness of the


risk factors that can affect the prognosis
ANATOMY OF THE JOINT
EPIDEMIOLOGY

• Most common arthropathy (accounts for ~75% of all arthritis)


• Increased prevalence with increasing age (35% of 30 yr olds, 85% of 80 yr olds)
• Affect mostly females
• DIP and PIP with Heberden and Bouchard – in females
• Middle aged to elderly : 45-65
• Uncommon less than 30
• 20 million in USA
• 1.5 million in U.K
• 9 million all arthritis UK
• 2nd to IHD as cause work disability in men >50yrs
• Constitutes about 80% of our rheumatology practice
• Radiologic changes osteophytes in 50% aged 65+
• Higher incidence in Afro American female and Japanese
• Low incidence – South African blacks, east Indians, Southern
Chinese
Burden of OA
• Anxiety
• Depression
• Helplessness
• Limitations of daily activities
• Job Limitation
• Economic – Direct and Indirect costs – appliances, lost wages, travel
costs
CLASSIFICATION(BASED ON ETIOLOGY)

Primary (idiopathic)
• most common, unknown etiology
Secondary
• post-traumatic or mechanical
• post-inflammatory (e.g. RA) or post-infectious
• heritable skeletal disorders (e.g. scoliosis)
• endocrine disorders (e.g. acromegaly, hyperparathyroidism,
hypothyroidism)
• metabolic disorders (e.g. gout, pseudogout, hemochromatosis,
Wilson’s disease, ochronosis)
• neuropathic (e.g. Charcot joints)
• atypical joint trauma due to peripheral neuropathy (e.g. diabetes
mellitus, syphilis)
• avascular necrosis (AVN)
• other (e.g. congenital malformation)
Risk factors
• genetic predisposition,
• advanced age,
• obesity (for knee and hand OA),
• female,
• trauma
PATHOPHYSIOLOGY

• The process appears to be initiated by abnormalities in


biomechanical forces and/or, less often, in cartilage
• Elevated production of pro-inflammatory cytokines(IL-1 & TNF-alpha)
are important in OA progression
• Tissue catabolism > repair
• Contributing factors (mechanisms unknown): genetics, alignment
(bow-legged, knock-kneed), joint
• deformity (hip dysplasia), joint injury (meniscal or ligament tears),
obesity, environmental, mechanical loading, age and gender
• Now considered to be a systemic musculoskeletal disorder rather
than a focal disorder of synovial joints
SOURCE OF PAIN

• Joint effusion – capsular stretch


• Subchondral bone – vascular distension – vasa nervorum
• Periarticular Bursitis
• Periarticular muscle spasm
• Damaged meniscus
• Tendon Stretch
PRESENTATION

• Pain - Use-related joint pain, relieved by rest, gradually progressive,


with intermittent flares and remission; In more advanced cases rest
pain and night pain can also develop
• Stiffness- Most people with symptomatic osteoarthritis of large joints
experience short-lasting inactivity stiffness or gelling of joints, which
wears off in a few minutes with use
• Reduced movement- The range of movement of the joint is often
restricted, and there is generally pain on movement, particularly at the
end of the range
• Swelling - Many osteoarthritic joints develop palpable firm swellings
at the joint margin due to the formation of osteophytes; some have
minor soft tissue swelling due to secondary synovitis

• Crepitus - Osteoarthritic joints often crack or creak on movement

• Fatigue, poor sleep, impact on mood (depression, anxiety)


JOINT INVOLVEMENT

• Generalized osteoarthritis: 3+ joint groups


• Asymmetric (knees usually affected bilaterally)
• Hand
 DIP (Heberden’s nodes = osteophytes → enlargement of joints)
 PIP (Bouchard’s nodes)
 CMC (usually thumb squaring)
 1st MCP (other MCPs are usually spared)
 OA of MCP joints can be seen in hemochromatosis or CPPD-related disease
(chondrocalcinosis)
• Hip
 usually presents as groin pain ± dull or sharp pain in the trochanteric area,
internal rotation and abduction are lost first
 pain can radiate to the anterior thigh, but generally does not go below the
knee
• Knee
 initial narrowing of one compartment, medial > lateral; seen on standing x-
rays, often patellar-femoral joint involved
• Foot
 common in first MTP and midfoot
• Lumbar spine
 very common, especially L4-L5, L5-S1
 degeneration of intervertebral discs and facet joints
 reactive bone growth can contribute to neurological impingement (e.g.
sciatica, neurogenic claudication) or spondylolisthesis (forward or
backward movement of one vertebra over another)
• Cervical spine
 commonly presents with neck pain that radiates to scapula, especially
in mid-lower cervical area (C5 and C6)
Common sites of joint involvement in OA

Hand findings in OA
INVESTIGATIONS

• Blood work
 normal CBC and ESR, CRP
 negative RF and ANA
 radiology: 4 hallmark findings,
• The Radiographic Hallmarks of OA
 • Joint space narrowing
 • Subchondral sclerosis
 • Subchondral cysts
 • Osteophytes-hallmark of OA
• However, clinical symptoms and radiograph findings are poorly
correlated, many joints with radiographic evidence of OA remain
asymptomatic and, conversely, the joints of many patients with
severe symptoms can appear only marginally affected on X-ray

• synovial fluid: non-inflammatory


• M.R.I
 MRI can be useful for excluding tumour, algoneurodystrophy or avascular
osteonecrosis.
 Cartilage thickness could precociously be detected by MRI.
 The pain and progression of knee OA seem to be associated with the bone
marrow edema seen on MRI, but this remains controversial
• Bone Densitometry
• Thermography
• Bone Scan
• Arthroscopy
DIFFERENTIALS

• RHEUMATOID ARTHRITIS
• GOUTY ARTHRITIS
• PSEUDO GOUT
• EROSIVE ARTHRITIS
• PSORIATIC ARTHRITIS
• TRAUMATIC SYNOVITIS
• FIBROMYALGIA SYNDROME
MANAGEMENT

• Objectives
• Patients education and information access
• Pain relief
• Optimisation of function
• Beneficial modification of OA process
• Management should be individualised
• Successful management requires the use of multiple components,
both non-pharmacological and pharmacological, rather than a
monotherapy approach
• Presently no treatment alters the natural history of OA
• Prevention: prevent sports injury, healthy weight management
• Team Approach – Rheumatologist, Physiotherapist, Occupational
therapist, nutritionist, orthopaedic surgeon
• Medical treatment- Rheumatologist
• Surgical treatment- Orthopaedic Surgeon
TREATMENT
Non-pharmacological therapy
Weight loss , if overweight
Assistive Devices – walking sticks, walking frame, bracing,
splints
Hydrotherapy
Physical exercises – walking, bicycling
Aerobic exercises – quadriceps strengthening
TENS
Infrared-popular but not effective
• Pharmacological therapy
 1st line- oral: acetaminophen
 2nd line - NSAIDs
 Treat neuropathic pain/Night pain if present (anti-depressants, anti-
epileptics, etc.)
 3rd line - Narcotic analgesic- tramadol, codeine. Transdermal opioids
 Joint injections: corticosteroid (effective for short-term treatment),
hyaluronic acid (evidence of long-term benefts)
• Topical: capsaicin, NSAIDs
• Food supplements-Glucosamine ± chondroitin sulphate (efficacy
not well supported)
• Acupuncture
• Surgical treatment
 Joint debridement, osteotomy, total and/or partial joint replacement,
fusion
ARTHROPLASTY
bad good
TAKE HOME

• Arthritis not one disease


• More than 200 types/causes
• Osteoarthritis very common.
• Oa knee particularly common in women
• Collaboration between rheumatologist, orthopaedic surgeon and para medical
personnel
• Paracetamol before nsaids
• No nsaid superior to another. Responses/ side effects vary
• Narcotic analgesics useful singly or combination
• thank you

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