THE ROLE OF MUSCLE WEAKNESS IN THE PATHOGENESIS OF OSTEOARTHRITIS

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Osteoarthritis (OA) is the most common form of arthritis to affect synovial joints.4, 5, 88 Although more benign than other rheumatic disorders, such as rheumatoid arthritis (RA), the personal cost in terms of pain and disability, the financial costs of its management, 88 and the prevalence4, 5 of this disease lead to serious socioeconomic consequences.46, 78, 88

Although there is a strong association between OA and mechanical abnormalities, and the prevalence of OA increases with age, 54 the explanation usually proffered to patients—that OA is an inevitable consequence of ageing because of the normal wear and tear of the joint—is too simplistic. It is becoming increasingly clear that OA is much more complex than previously thought.

Rather than being viewed as a single pathologic entity, OA is better regarded as subsets of joint disorders, with different causes (e.g., mechanical, hormonal, or genetic), but that share common pathologic processes that result in similar alterations in articular anatomy and function and have common clinical features.63 The principal clinical features reported by patients are joint pain, decreased function, joint instability, periarticular muscle weakness, and fatigue. The onset of these symptoms is almost invariably insidious, with episodes of pain that increase in frequency and duration until, eventually, the patient may be in constant pain.

A diagnosis and categorization of the severity of OA is frequently made from radiographic evidence of attrition of the articular cartilage and changes in the underlying subchondral bone. Research in OA has focused mainly on the intra-articular changes and has revealed a great deal about the pathophysiologic processes that occur within the articular milieu. In contrast, there has been very little research interest in the changes that take place in the periarticular skeletal muscles17; however, muscles are integral to joint function and the synovial joint should be considered a functional unit of the neuromuscular skeletal system, which is composed of the articulating bones, cartilage, ligaments, capsule, the muscles that effect movement, and the nerves that control movement. Accurate, controlled movement relies on each component of these units working optimally. If any component is dysfunctional, the joint will be dysfunctional. The limited number of research studies that have been performed in this area have led to an appreciation of how muscle is affected by the condition, and to growing conjecture that muscle dysfunction may be involved in the pathogenesis of OA.17, 57, 112, 116

This article presents some of the studies that implicate motor dysfunction as a cause in the pathogenesis of OA and touches on the sensory function of muscle, which is intimately linked with motor function. It also cites the results of studies demonstrating the efficacy of rehabilitation in reversing sensorimotor dysfunction to reinforce the argument that muscle plays a vital role in OA. This article should be considered, therefore, in association with two other articles in this issue, “Proprioceptive Impairment in Knee Osteoarthritis” by Dr Leena Sharma, and “Exercise in the Treatment of Osteoarthritis” by Dr Marian Minor, which provide more inclusive reviews of these areas. The present article concentrates on knee OA because most of the work studying muscle dysfunction in OA relates to knee OA in particular, largely because the knee musculature is relatively easily investigated. The choice is easily justified, however, because the knee is the joint most frequently affected by OA and knee OA the most common cause of disability among the elderly. Knee OA is a major public health problem and warrants concern and research attention.

Section snippets

Movement

The purpose of a synovial joint is to enable an individual to move and interact with his or her environment. Force generation and movement are effected by contraction of the skeletal muscles that span the joint. Muscle contractions may be concentric (the muscle shortens and moves the joint), eccentric (the muscle lengthens but still maintains tension and controls the movements of the joint) or isometric (the muscle contracts but joint movement is prevented by an opposing force).

Functional Joint Stability

Another

CONTROL OF MUSCLE FUNCTION

Skeletal muscle activity is controlled and innervated by peripheral motor nerves that are comprised of α-motoneurones. Excitability of α-motoneurones is influenced by the supraspinal motor centers of the CNS, segmental spinal interneurons, rhythmic movement pattern generators, involuntary reflexes and sensory input from proprioceptors in muscle, articular structures, and skin.2, 6, 66, 83, 84, 93 Factors that decrease the excitability of α-motoneurones reduce muscle activation and decrease

THE ARTICULAR CONSEQUENCES OF MUSCLE DYSFUNCTION

It is usually assumed that articular damage elicits pain and effusion that can be improved by rest or decreased joint use, but this therapeutic approach exacerbates the weakness (Fig. 1).119 Weak muscles are fatigued more readily, and their voluntary and reflex motor control is slower than those of well-conditioned muscles. This motor dysfunction compromises the neuromuscular protective mechanisms of the muscle, leading to excessive joint movement and instability, which stresses innervated

Lack of Association Between Radiographic Evidence of Joint Damage, Muscle Weakness, Pain, and Disability

A poor association exists between radiographic signs of joint damage and the joint pain and disability experienced by a patient with OA; some patients with severe radiographic joint damage complain of little pain or may even be asymptomatic, whereas others with severe pain may exhibit only minor degenerative changes.21, 91 Conversely, quadriceps weakness is one of the commonest and earliest symptoms reported by patients41, 42, 43, 60, 79, 85 and is a better determinant of pain and disability

CAN QUADRICEPS SENSORIMOTOR DEFICITS BE REVERSED?

That changes in muscle sensorimotor dysfunction are involved in the pathogenesis and progression of OA may be good news. At present, little can be done to reverse damage to articular structures or subchondral bone. Surgical intervention and drug therapy can reduce pain and improve function, but their availability is limited, they are expensive, they can have serious side effects and risks, and they are initiated only after the symptoms and radiological damage are well established. Even when

A MODIFIED PARADIGM OF THE INTERRELATIONSHIP BETWEEN MUSCLE DYSFUNCTION, JOINT DAMAGE, AND DISABILITY

It is assumed joint damage initiates the proposed vicious circle of events that leads to decreased activity and muscle weakness (exacerbated by arthrogenic reduction in voluntary activation), which increases the risk of secondary joint damage (see Fig. 1).119 Based on the preceding arguments and evidence, the author contends that the initiation and progression of the pathological processes in OA are not so straightforward (Fig. 2). The pathologic processes may be initiated by sensorimotor

ACKNOWLEDGEMENT

The author would like to thank the Arthritis Research Campaign, which generously funded much of this work.

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    Address reprint requests to Michael V. Hurley, PhD, MCSP, Rehabilitation Research Unit, Physiotherapy Division, King's College London, King's Healthcare (Dulwich), East Dulwich Grove, Dulwich, London, SE22 8PT, UK, [email protected]

    *

    Rehabilitation Research Unit, Physiotherapy Division, King's College London, King's Healthcare, Dulwich, London, United Kingdom

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