Page 362 - Medicine and Surgery

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358 Chapter 8: Musculoskeletal system

Table 8.3 Causes of secondary osteoarthritis the disease progresses, pain occurs with less activity and
eventually occurs at rest. Stiffness occurs after a period of
Structural change Intra-articular fracture, joint
malalignment, joint hypermobility, rest, but is less severe than rheumatoid arthritis and lasts
congenital dysplastic hips, 5–15 minutes in morning. On examination there may be
Perthes’ disease joint line tenderness, joint effusion, crepitus and bony
Inflammatory joint Septic arthritis, rheumatoid arthritis, enlargement due to osteophyte development. There is
damage repeated haemarthrosis in gradual limitation of movement with resultant muscle
haemophilia
Genetic collagen Mutations in type II collagen genes wasting and deformity.
disorders resulting in increased susceptibility Hands: An enlargement of the distal (Heberden’s
to damage nodes) and proximal interphalangeal (Bouchard’s
Calcium deposition Chondrocalcinosis nodes) joints results in a square appearance of the
disorders
hands. The development of Heberden’s nodes appears
to have a genetic predisposition.
Feet/ankles: The first metatarsophalangeal joint is
Aetiology
commonly affected; subtalar joint involvement may
Primary osteoarthritis: Risk factors include obesity,

cause difficulty with walking.
increasing age, female sex, wear of cartilage through
Knees: The medial part of the knee joint may be af-
repeated trauma.
fected more than the lateral causing a genu varum.
Secondary osteoarthritis: Osteoarthritis may result

Knee involvement often results in osteophyte forma-
from damage to the joint or changes to the way forces
tion,jointeffusion,crepitusandaBaker’scystpalpable
are transmitted through the cartilage (see Table 8.3).
in the popliteal fossa.
Pathophysiology Hips are commonly affected, although some apparent
Normal cartilage consists of chondrocytes, collagen and hip pain may be referred from other areas.
extracellular matrix. The damage seen in osteoarthritis Spine: Particularly the cervical and lumbar region.
is initiated by trauma, which may be a single event or
repeated microtrauma. Any underlying collagen defect
Investigations
will predispose to damage. There is resultant increased
The first radiological finding is narrowing of the joint
proliferation and activity of chondrocytes under the in-
space. In weight-bearing joints narrowing is maximal
fluence of monocyte-derived growth peptides. Once the
in the areas subjected to the greatest pressures. As the
process of osteoarthritis has begun a number of factors
cartilage is worn away, friction causes the exposed sub-
are involved in the continued disease process:
chondral bone to become sclerotic (subarticular bony
Mechanical forces can be causative, preventative or

sclerosis). The presence of bone cyst formation is a com-
therapeutic.
mon finding. Later findings include bony collapse and
Proteases that are involved with cartilage degradation.

the formation of osteophytes (bony outgrowths that are
Ithasbeensuggestedthatproteaseactivationisimpor-
seen at the margins of the joint). Inflammatory markers
tant.
and autoantibodies are negative.
Cytokines including IL-1 and TNF-α,havearole in

cartilage degradation. Growth factors mediating col-
lagen repair include insulin-like growth factor and Management
transforminggrowthfactorβ (TGF-β),whichreduces 1 Non-pharmacological management includes weight
the activity of proteases and therefore limits cartilage loss, physiotherapy, walking aids and hydrotherapy to
degradation. rebuild lost muscle bulk.
Other factors implicated include crystals and nitric
2 Medical treatments are used for pain relief. Sim-
oxide. ple analgesia and nonsteroidal anti-inflammatory
drugs are the mainstay of treatment supplemented
Clinical features by intra-articular steroid injection. See also indica-
Patients tend to present with gradual onset of joint pain, tionsforCoxIIantagonistsunderrheumatoidarthritis
which is exacerbated by exercise and relieved by rest. As (page 360).