Материал: ABC-of-Rheumatology-ABC-Series-

Arthritis (2005) in the

United States

(a)

People with Arthritis 1990 and 2005

1990

2005

By 2030, as the baby boom generation ages, an estimated 75 million Americans will be affected by arthritis.

Leading Causes of

Disability Among Persons

Age 18 Years and Older

Arthritis or rheumatism

Back or spine problem

Heart trouble

Lung or respiratory problem

Deafness or hearing problem

Limb/extremity stiffness

Mental or emotional problem

Diabetes

Blindness or vision problem

Stroke

Percentage of all disability

Men

OA prevalence (%)

Women

OA prevalence (%)

Age (yrs)

Pathways to osteoarthritis

Cell/matrix injury

Aberrant repair response

Enzymatic degradation

Collagen disruption

Proteoglycan loss

Mechanical failure

Figure 9.2 Pathways to osteoarthritis. Taken from Poole et al. 2007, with permission of Dr Farshid Guilak and the publisher, Lippincott Williams & Wilkins

Aetiology of osteoarthritis and rheumatoid arthritis

Figure 9.3 Aetiologies of OA and RA

Table 9.1 Important risk factors for osteoarthritis

resting (“gelling”), in the absence of systemic symptoms (fatigue, fever) or other system involvement. Joint stiffness arises, at least in part, from the accumulation of hyaluronan (a joint lubricant and the most abundant constituent of synovial fluid) and hyaluronan fragments in the deep layers of arthritic synovium during periods of rest, excluding water within the synovial tissue. Joint movement mobilizes hyaluronan from the tissue to the lymphatics and blood with attendant hydration of synovial tissue and improvement in joint stiffness symptoms (Engstrom-Laurent, 1987). The cartilage changes that accompany OA encourage deposition of crystals— both calcium crystals (calcium pyrophosphate and basic calcium phosphates), especially at the knee, and urate crystals. Patients with OA may therefore develop superadded acute pseudogout (mainly knees and wrists), and are at increased risk of secondary gout if they are on long-term diuretics or have chronic renal impairment (see Chapter 10).

Distribution of primary OA and RA

Figure 9.6 Hands with Heberden’s nodes (bony enlargement of distal interphalangeal joints) and Bouchard’s nodes (bony enlargement of proximal interphalangeal joints)

Examination

The main clinical features of OA are symptoms, functional impairment and signs. Considerable discordance can exist between these three (Figure 9.8). Pain may arise from several sites in and around an osteoarthritic joint (Table 9.2). Suggested mechanisms include increased intra-capsular and intra-osseous pressure, subchondral microfracture and enthesopathy or bursitis secondary to muscle weakness and structural alteration. Severity of pain and functional impairment are greatly influenced by personality, anxiety, depression, daily activity and reduced muscle strength and proprioception (muscle performs an important proprioceptive role).

OA

RA

Figure 9.5 Pattern of joint distribution of primary OA and RA

40

30

20

10

0

Age class

Figure 9.7 Prevalence of knee OA after injury compared with baseline risk. Taken from Roos, 2005, with permission of Dr Ewa Roos and the publisher, Lippincott Williams & Wilkins

Table 9.2 Types of joint pain in OA

Figure 9.8 The discordance between radiographic OA and symptoms in the hands (distal interphalangeal joints, knees and hip). Taken from Arden and Nevitt, 2006, with permission of Drs Nigel Arden and Michael Nevitt and the publisher, Elsevier

Crepitus, bony enlargement, deformity, instability and restricted movement may occur together and predominantly reflect structural changes. Varying degrees of synovitis (warmth, effusion and synovial thickening) may be superimposed, especially noticeable in knees, and muscle weakness or wasting is extremely common.

Assessment aims to establish the source of symptoms in each patient. When diffuse and generalized tender points are identified at tendon insertion sites, then the co-occurrence of fibromyalgia should be considered and attention to improving sleep be included in the management considerations. Only an adequate history and examination can determine how much structural and inflammatory change is present and how much these contribute to a patient’s problems.

Box 9.1 European and US Guidelines for management of OA

•The management plan must be individualized, taking into account the site and severity of OA symptoms, any co-morbidity, concurrent medications and patient acceptability

•Non-pharmacological treatments are central—drug treatments are adjuncts

•A core and option approach is required—all patients should be offered education, an exercise programme, advice to reduce adverse mechanical factors and paracetamol as the first oral analgesic to try; there is a wide range of other treatment options from which to select additional treatments, as required

Diagnosis

Typical OA can be diagnosed by history and examination alone. Currently the main investigation that can help confirm OA is the plain X-ray, with demonstration of characteristic structural abnor- malities—focal joint-space narrowing (due to cartilage loss), marginal osteophyte or “spur” formation and subchondral sclerosis of bone (Figure 9.9). It is increasingly recognized that biochemical abnormalities of the joint precede radiographic abnormalities by as much as decades. For this reason, much effort is currently being put into identifying more sensitive imaging modalities, such as magnetic resonance imaging, bone scintigraphy and ultrasound, along with biochemical indicators in blood, urine or synovial fluid, that might identify and quantify OA more precisely and earlier than by X-ray.

Management

The goals of medical management of OA (summarized in Figure 9.10) are to: (a) provide patient education and information access;

(b) relieve pain; (c) optimize function; and (d) minimize disease

progression. See Box 9.1 for European and US guidelines on management of OA.

Symptoms of OA often are episodic. It is therefore advisable to provide the patient with an armamentarium of treatment options to choose from during periods of relative quiescence and relative flare.

Patient education and information access

This is a professional responsibility, but education also improves outcome and is a treatment in its own right. The myth that OA is a progressive wearing-out of joints due to old age still persists; this invariably leads to inappropriate reductions in activity. A major contribution to managing OA has been the finding that a patient’s psychological status (anxiety, depression and social support) is an important determinant of symptomatic and functional outcome. Good evidence supports the use of educational programmes to help patients understand OA and develop self-management strategies.

(a)

Hip joint

(b)

Tibiofemoral knee joint

Patellofemoral knee joint

Sclerosis

Joint-space narrowing

Joint-space narrowing

Osteophyte

Sclerosis

Osteophyte