This document provides an overview of osteoarthritis (OA), including its definition as a disease affecting synovial joints marked by cartilage loss and bone changes, leading to pain and impaired movement. It discusses the epidemiology of OA as the most common form of arthritis. The document outlines various causes and clinical subsets of OA and describes the pathological process involving breakdown of collagen and proteoglycans in cartilage. Diagnosis involves history, physical exam, and imaging tests. Treatment options discussed include lifestyle changes, medications, and surgeries such as joint replacement or resurfacing.

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Osteoarthritis
Fadi Hassan – Hull York Medical School

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Overview
 Definition
 Epidemiology
 Aetiology
 Signs and symptoms
 Pathogenesis
 Clinical Subsets
 Investigations
 Treatment options

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Definition
“Disease of synovial joints marked by
cartilage loss and peri-articular bone
response. It usually affects the wrist, hip,
knee and the ankle joint. It causes the
bones to be exposed and damaged
leading to pain and impaired movement”

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Epidemiology
 OA is the most common type of arthritis as prevelance
increases with age.
 Leading cause of chronic disability affecting 8 million people in
the UK and 27 million in the US.
 Women over the age of 55 are affected more than men of a
similar age.
 Associated with major socio-economic implications especially
in developed countries.

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Aetiology
 Can be classified as
 Primary
 Secondary
 Or as
 Hereditary
 Developmental
 Metabolic
 Mechanical

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Primary OA
 Could be related to aging
 Reduced proteoglycan content leading to the joint being less
resilient and more susceptible to degradation speeding up the
process of degeneration.
 Genetic
 Twin studies shown that there is a greater prevalence of the disease
in siblings and specifically identical twins (more than 60%)

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Secondary OA
 Obesity
 Injury to joints/ligaments
 Ligamentous instability
 Congenital abnormalities
 Diabetes
 Septic arthritis
 Inflammatory diseases (gout,
lyme disease)
 Alkaptonuria (black urine)
 Ehlers-Danlos syndrome (EDS)
 Hemochromatosis
 Wilson’s disease

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Secondary OA - Alkaptonuria
 Inherited disorder of phenylalanine and tyrosine
metabolism as a result of enzymatic defect leading
to accumulation of alkapton (homogentisic acid
and its oxide) in blood/urine
 Excess homogentisic acid causes damage to
cartilage tissue.

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Secondary OA - EDS
“Connective tissue disorder causing
defects in the synthesis of collagen (I/II)
that in normal situations help in resisting
deformation and maintains the connective
tissue elasticity”

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Pathogenesis
 Collagen matrix degeneration is mediated by the action of
Matrix MetalloProteinases like
 Collagenase (MMP1 and MMP13) by cleaving collagen
 Stromelysin (MMP3) which is active against fibronectin and laminin
in the extracellular matrix.
 MMPs are secreted by chondrocytes in an inactive form which
leads to degeneration of collagen and proteoglycan upon
extracellular activation.
 The role of Tissue Inhibitors of Metalloproteinases
 TIMPs play a role in regulating MMP production and any
disturbance in this pathway leads to cartilage degradation

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Pathogenesis
 Deficiency of growth factors (IGF-1) and transforming growth factor
(TGF-B) play a role in impairing matrix repair as a result of reduced
collagen synthesis.
 Other mechanisms?
 Genetics: Mutations in the gene for type II collagen (COL2A1)
have been associated with early OA
 Vitamin C and antioxidants deficiency

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Synovial Inflammation
 As breakdown products from the cartilage are released into the
synovial space, the cell lining the joint will try and remove them
leading to an inflammatory response.
 Cytokines production regulates cartilage damage
 Interleukin-1 and tumour necrosis factor release stimulates
metalloproteinase
 Interleukin-6 and Interleukin-8 may also be involved.
 NF-KB transcription factor mediates the production of cytokines
and MMPs.

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Clinical subsets
 Localized OA
 Nodal (joints of the hands – DIPs >PIPs)  Pain + swelling = functional
impairment
 Hip: occurs most frequently at the superior pole of the hip where there is
joint space narrowing and sclerosis affecting the upper surface of
femoral head and acetabulum.
 Knee: medial compartment > lateral compartment
 Can be retropatellar
 Primary generalized: main characteristics are
 >1 joint, familial tendency, female predominance and autoimmune
association
 Erosive: DIPs and PIPs  subchondral cysts developing into RA
 Crystal-associated (calcium pyrophosphate deposition)
 Chondrocalcinosis characterized by patchy linear calcification on x-ray

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Patchy linear calcification

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Diagnosis and clinical features
 History
 Sharp aching pain and stiffness
 Burning sensation in the muscles or tendons
 Usually affects the hands, feet, spine, hip and knee
 Humid and cold weather usually exacerbates the symptoms
 Gets better with gentle use but worsens on excessive use
 Main principle that distinguishes OA from RA

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Diagnosis and clinical features
 Examination
 It can cause crackling noise (crepitus) on moving the joint
 Associated locking
 Muscle atrophy
 Lax ligaments
 Joint effusion
 Heberden’s nodes (DIP) and/or Bouchard’s nodes (PIP) limiting
movement of the joints
 OA of the toe leads to formation of bunions

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Diagnosis and Clinical features
 Investigations
 X-ray:
 Joint space narrowing
 Subcondral sclerosis
 Osteophyte formation
 Subcondral cyst formation
 Blood tests
 Raised CRP (in some cases)
 Normal ESR
 Rheumatoid factor and antinuclear antibodies are negative
 MRI: early cartilage and subcondral bone changes, although it is not
routinely used due to the cost
 Arthroscopy can reveal early fissuring and surface erosions

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Imaging

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Imaging

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Treatment
 Lifestyle modification
 Weight loss
 Patient education
 Moderate exercise
 Manual therapy (manipulation of muscles and joints)
 Medications
 Surgical approach:
 Considered if non-surgical treatment lose their effectiveness in pain management
 Age, activity level and the condition of affected joints are all factors that should be
considered
 Accupuncture
 Supplements (multivitamins, ginger, Omega-3-FA)

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Treatment
 Medications
 Acetaminophen (COX inhibitor) is usually the first line of treatment and
is recommended for mild-moderate symptoms
 NSAIDs like ibuprofen are more effective for severe symptoms.
However, they’re associated with greater side effects like GI bleeding
 COX-2 selective inhibitors (celecoxib) is associated with less side
effects but higher rates of CV diseases
 Topical NSAIDs like diclofenac could be used
 Opioid analgesics such as morphine improve pain but have greater side
effects.
 Steroids (hydrocortisone) achieve short term pain relief but they have
side effects
 Osteoporosis, weight gain, infections, HTN, diabetes, skin thinning,
muscle weakness, mood and behavioural changes, cataracts and
stomach ulcers

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Treatment
 Surgical approach
 Arthroplasty (joint replacement)
 Parts of the bones are removed and artificial joint with metallic or plastic
components are created
 Joint resurfacing ( metal-on-metal articulation)
 Placing a metal cap over the reshaped articular surfaces removing very little
bone compared to arthroplasty
 Revision is easy with this option as the bone is preserved so other procedures
can still be considered in the future (like arthroplasty)
 Arthroscopy
 Arthroscope is used to remove bone spurs, cysts and damaged surfaces from
the joint.
 Osteotomy
 Involves realignment of the long bones to ease off the pressure on the joints
 Joint fusion
 Fusion both ends of the bone together and holding them in place using pns,
plates or screws while they heal.
 This procedure usually sacrifices the joint’s flexibility