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Musculoskeletal Function
is mild, and the person seeks medical care only with the
onset of definite arthritis. Short antibiotic courses at this
time are not effective.
Psoriatic Arthritis
Psoriatic arthritis is a seronegative inflammatory arthrop-
athy that occurs with variable frequency in people with
psoriasis.
56–58
It is a disease with various and similar fea-
tures of the spondyloarthropathies in some persons, in
whom an asymmetric sacroiliitis and spinal involvement
predominate. In others, the disease is polyarticular and
resembles RA, and in some, features of both disorders
coexist. Although the arthritis can antedate a detectable
skin rash, the definitive diagnosis of psoriatic arthritis
cannot be made without evidence of skin or nail changes
typical of psoriasis (see Chapter 46).
The etiology of psoriasis and psoriatic arthritis is
unknown. Genetic, environmental, and immunologic
factors appear to affect susceptibility and play a role in
expression of the psoriatic skin disease and the arthri-
tis. Environmental factors that may play a role in the
pathogenesis of the disorder include infectious agents
and physical trauma. T-cell–mediated immune responses
seem to play an important role in the skin and joint man-
ifestations of the disease, as indicated by the observation
that there is improvement in disease status after treatment
with immunosuppressant agents such as cyclosporine.
Psoriatic arthritis falls into five subgroups: (1) an
oligoarticular form affecting four or fewer joints;
(2) a spondylitis form in which sacroiliitis and spinal
involvement predominate; (3) a polyarticular, or sym-
metric, form that resembles RA; (4) a form in which
the distal interphalangeal joints are primarily affected;
and (5) arthritis mutilans, a very destructive form of
arthritis.
56,57
The joint involvement of peripheral psori-
atic arthritis is inflammatory in nature, presenting with
swelling and stiffness of the affected joints. Early in the
disease, the arthritis tends to be oligoarticular, but may
become polyarticular over time. The affected joints of
persons with psoriatic arthritis are often less tender than
those of persons with RA. Thus, persons with psoriatic
arthritis may present with deformity and joint damage,
not having perceived any pain during the inflamma-
tory phase of the disease. Sacroiliac involvement, when
it occurs, tends to be asymmetric, involving only one
sacroiliac joint and sparing the other or with differ-
ent degrees of radiologic involvement. Likewise, spinal
involvement tends to be asymmetric, with skip lesions.
Dactylitis
, or
sausage digit
, is a typical feature of distal
interphalangeal joint disease and reflects inflammation
of the entire digit.
56,57
Basic management is similar to the treatment of RA.
Suppression of the skin disease may be important in
helping control the arthritis.
56–58
Often, affected joints
are surprisingly functional and only minimally symp-
tomatic. The biologic response modifiers, specifically
the TNF inhibitors (e.g., etanercept, infliximab, and
adalimumab), have been found to be beneficial in con-
trolling the arthritis as well as the psoriasis in patients
with psoriatic arthritis.
56
Osteoarthritis
Osteoarthritis (OA), also called
degenerative joint dis-
ease,
is the most prevalent type of joint disease and is
one of the 10 most disabling conditions in developing
nations.
3,4
The disorder, which is characterized by degen-
erative changes of the articular cartilage, can affect any
one of 200 or so synovial joints in the body, and can
occur as a primary idiopathic disorder or as a second-
ary disorder. In most instances, OA appears insidiously,
without an apparent initiating cause, as an aging phe-
nomenon (idiopathic or primary OA).
3,4
In these cases
the disorder is usually oligoarticular, but may be gen-
eralized. Secondary OA has a known underlying cause
such as congenital or acquired defects of joint structures,
trauma, metabolic disorders, or inflammatory diseases.
Joint changes associated with OA include a gradual
loss of articular cartilage, combined with thickening of
the subchondral bone, bony outgrowths (osteophytes)
at joint margins, and mild synovial inflammation. These
changes are accompanied by joint pain, stiffness, and
limitation of motion, and in some cases by joint instabil-
ity and deformity.
Etiology and Pathogenesis
Osteoarthritis is a multifactorial disease that has genetic
and environmental risk factors. Studies of families and
twins suggest that the risk of OA is related to the net
impact of multiple genes, each with a small effect.
3,4
Age, gender, and race interact to influence the time of
onset and the pattern of joint involvement in OA. Age
is one of the strongest risk factors for OA of all joints.
The increase in incidence and prevalence with age prob-
ably is the consequence of cumulative exposure to the
various risk factors and biologic changes that occur in
a life time. Women are more likely to have OA than
men, and they tend to have more severe OA as well. The
prevalence of OA and pattern of joint involvement vary
among racial and ethnic groups. Hand OA is more likely
to affect white women, whereas knee OA is more com-
mon in black women. The incidence of hip OA is lower
among the Chinese than Europeans, perhaps represent-
ing the influence of other factors such as occupation,
obesity, or heredity. Bone mass may also influence the
risk of developing OA. In theory, thinner subchondral
bone mass may provide a greater shock-absorbing func-
tion than denser bone, allowing less direct trauma to
the cartilage. Obesity is a particular risk factor for OA
of the knee in women and a contributory biomechani-
cal factor in the pathogenesis of the disease. Weight loss
reduces the risk of developing symptomatic arthritis of
the knee.
The pathogenesis of OA resides in the homeostatic
mechanisms that maintain the articular cartilage.
3,4,59
Articular cartilage plays two essential mechanical roles in
joint physiology. First, it serves as a remarkably smooth
weight-bearing surface. In combination with synovial
fluid, the articular cartilage provides extremely low fric-
tion during movement of the joint. Second, the carti-
lage transmits the load down to the bone, dissipating
