Hand osteoarthritis

Introduction

An emerging view of osteoarthritis (OA) is renewing interest in the role of physical activity in OA and the clinical correlate, the potential for change in physical activity to stem OA progression and, possibly, restore joint function. The purpose of this report is to present a view of hand OA as cumulative microtrauma mediated by physical activity. The view was derived from insights from a wide range of sciences and professions, laboratory and clinical research models, and expert opinions. Grounded in principles of hand pathomechanics, the view places physical activity at the centre of the process through which problems in the joint (originating from many possible sources) result in a cascade of symptoms and hand impairments.

OA overview

A common form of OA in the hand is nodal or generalized OA affecting the interphalangeal (IP) and carpometacarpal (CMC) joints. Diagnosis can usually be based on history and physical exam. ¹ The symptoms are activity-related joint pain and short-lasting joint stiffness after inactivity, accompanied by soft tissue swelling, bony enlargement, weakness, crepitus, local inflammation, deformity and functional limitations. ^1–3 The loss of articular cartilage, bony overgrowths on joint margins (osteophytes) and changes in subchondral bone are also diagnostic. ¹ Symptomatic hand OA tends to affect multiple hand joints, to cluster by row (joint) rather than ray (phalanx), and to occur in symmetrical patterns. ⁴ Hand OA in older adults is highly prevalent and a major cause of hand functional impairment. ^5,6

As in all OA, hand OA is believed to result from the interplay between systemic susceptibility (e.g. genetic, hormonal, nutritional and metabolic) and local joint factors (e.g. mechanical, traumatic and functional). ^7,8 The main predictors of hand OA are age, genetic predisposition and sex. ⁹ Risk factors for hand OA are many, varied, specific to joint and population subgroup, and debated. For a recent review of risk factors for hand OA, see Kalichman and Hernandez-Molina. ⁹

Development of hand dysfunction

Physical activity – defined as goal-directed, voluntary, neuromuscular action – maintains the structural and functional integrity of the joint tissues (cartilage, subchondral bone, ligaments, tendons, capsule, synovium, nerves and bridging musculature) and facilitates the development of neuromuscular joint protective and regulatory control mechanisms. Without physical activity of sufficient intensity, duration, frequency and variety, joints weaken and stiffen, and hand function deteriorates.

Physical activity in the hand generates force on the joint through the pull of working muscles on the joint tissues and through the application of external resistance or loads to the working muscles. The muscular forces, which produce most of the force, may be high because of relatively powerful finger flexors and relatively small joint surface areas leading to high force per unit area. ¹⁰

In the well-functioning joint, the loading and unloading of joint tissues through movement stimulates an ongoing process of tissue breakdown and repair (re-modelling) that maintains or enhances tissue integrity and joint function. Excessive force is absorbed and the joint is protected from damage by cushioning from articular cartilage, subchrondral bone and synovial, and other soft tissues.

Theoretically, the load-bearing capacity in the joint may be impaired by many factors, including cartilage, bone, muscle or connective tissue pathology, joint pathomechanics due to abnormalities in joint architecture, sensory disturbances or faults in neuromuscular control (micro-incoordinations or microklutziness ¹¹ ).

When the forces acting on a joint are extreme, injury occurs, such as tendon rupture or cartilage and bone fractures (trauma). However, subtraumatic level loads cause microtrauma to cartilage and bone that may exceed the ability of the joint to repair itself. Brandt and colleagues ^1,12 view OA as the process that is attempting to repair the damage caused by the excessive or faulty mechanical stresses on tissues. In this hypothesis, the formation of osteophytes and thickening of the capsule are attempts of the joint to splint itself, and the development of subchrondral bone lesions, which alter joint shape, are attempts to normalize load bearing. ¹ Muscle weakness, reflex inhibition and joint stiffness impair the joint load-bearing capacity, but also physiologically limit the force-generating capacity, thereby reducing loads on joint surfaces.

The local inflammatory response with OA (synovial effusions accompanied by joint redness/warmth and soft tissues swelling) is thought to be a secondary repair response stimulated by the biochemical breakdown products from the bone and cartilage re-modelling. ¹² Inflammatory mediators, however, may contribute to progression of joint structural changes in OA, ¹³ neural mediated bilateral OA expression ¹⁴ and joint hypersensitization. ¹⁵ Chronic inflammation may result from the OA-related joint tissue pathologies. ¹⁶

The causes of joint pain are not well understood. Typically, OA pain occurs with physical activity and is relieved by rest, but night pain and pain at rest may occur at any stage. Hand OA may be asymptomatic, and the severity of joint pathology may be discordant with the severity of pain. In end-stage OA (total joint destruction), pain may diminish or remit.

Pain in OA is likely initiated and sustained by a mix of articular, inflammatory and neurogenic factors. OA pain may originate in many different joint tissues and through different mechanisms including subchondral bone (medullary hypertension, microfractures), osteophytes (stretching of nerve endings in periosteum), ligaments (stretch), entheses (inflammation), capsule (distension, inflammation), periarticular muscle (spasm) and synovium (inflammation). ¹⁰ At the biochemical level, the joint structural re-modelling and inflammatory processes may interact to induce neurogenic changes in the articular, spinal and central pain pathways. In the OA joint, sensory fibers may increase in sensitivity, firing at lower thresholds, across wider fields and with less discrimination. ¹⁷ Cortically derived pain (sensorimotor incongruence) is also hypothesized as a potential source of pain in OA. ¹⁸ Following OA pain onset, cognitive and affective factors may come into play, further increasing the severity of the OA pain experience. ¹⁷ For discussions of modern theories of OA pain etiopathology, see Felson and Schaible ¹⁹ and Hunter et al. ¹⁷

Joint stiffness in OA is also not well understood. ¹ Joint stiffness tends to occur after inactivity, to be experienced as a gelling feeling, and may vary throughout the day. ²⁰ The causes of stiffness are unknown, although sensory disturbances have been hypothesized. ¹⁸

Decrements in hand function in OA also have complex etiologies and are the result of interactions among the evolving damage to the articular joints, adaptations to pain, weakness and stiffness, and changes in physical activity habits and patterns.

Age-related changes in immunological efficiency may diminish the efficiency of the repair processes, and age-related changes in neuromuscular, musculoskeletal and sensorimotor system functions (e.g. muscle weakness, connective tissue stiffness and prolonged reflexes) may increase joint vulnerability to force, alter joint mechanics and alter habitual physical activity. Thus, ageing contributes to the onset and progression of OA, but ageing is not a primary causal factor in the sense of OA as an inevitable consequence of tissue senescence. Some of the changes in aged articular cartilage are qualitatively different from those of osteoarthritic cartilage, ²¹ although the distinctions may be subtle. ²²

Early in the 20th century, Pommer first deduced the role of mechanical stress in cartilage degeneration from morphological analyses. ²³ In recent decades, the role of mechanical factors in OA has accrued through study of the mechanobiology of cartilage and bone, ^12,22,24 and is consistent with emerging evidence that suggests that OA is not primarily a disease of cartilage. ^25,26 In theory, the joint tissues damaged by force may be essentially healthy with a capacity to heal, if the stressors are removed. ¹² Although cartilage, the primary tissue involved in the process, does not heal, the abnormal cartilage produced by the re-modelling process, in some instances, may permit adequate joint function. ¹²

Although relatively few and highly varied, clinical studies of causal mechanisms in hand OA tend to support a role for functional, mechanical or mechanical mediating factors. Selected aspects of hand OA have been reported to correlate with small joint collateral ligament and tendon abnormalities, ²⁷ trapeziometacarpal subluxation, ²⁸ articular hypermobility, ²⁹ strength ³⁰ and hand usage patterns. ^9,31,32 In the absence of movement, as in hemiplegia, Heberden's nodes (distal IP swellings) do not develop. ¹⁴

An assumption of a causal relationship between joint stress and OA hand impairments underlies clinical principles and techniques for joint protection; the reduction or re-alignment of the forces operating on a joint is often one of the goals of hand therapy. Therapies that act, at least in part, to re-distribute or reduce loads on joint surfaces have been shown to reduce symptoms and possibly OA progression in both large (knee) ³³ and small (CMC) joints. ^34,35

Nothing in the view of OA described above dictates that the pathophysiological process must be inherently degenerative. OA becomes degenerative because the joint stressors that cause the problems – the adverse situations and joint environments in which the joint functions – continue to operate, and because the results of the failed re-modelling process – the observable features of OA – compound the problems.

Some thoughts on clinical intervention and research

Individuals with OA of the hand typically seek professional treatment when they experience symptoms, usually pain and difficulty performing functional activities. Conservative therapy for hand OA includes a range of treatment modalities, local rather than systemic, and individualized to the specific patient circumstances. ³⁶ Customary, conservative therapy typically includes some combination of medication targeting pain receptors and/or inflammatory mediators, supportive splinting, local joint rest, exercise for mobility and strengthening, instruction in adaptive techniques for improving function, provision of assistive devices, and training in principles of joint protection. ^35,37–39 Empirical support for conservative therapies in hand OA to control symptoms is limited, but generally encouraging. ^40–44 Conservative therapies have been incorporated into the EULAR-recommended guidelines for hand OA management. ³⁶ EULAR guidelines for joint protection and exercise for treatment of hand OA in primary care are being tested. ⁴⁵ Many people, however, either do not seek help for their hand OA or treatment offered may not be satisfactory. ⁴⁶ A typical lifetime course may involve recurrent bouts of pain and progression to joint deformity and functional impairments.

Effective hand therapy hinges upon remission of OA symptoms, particularly relief of pain, but unless the underlying symptom provoking conditions are addressed, symptoms may, over time, progress.

If, as hypothesized, the myriad of causal factors in OA are mediated by physical activity – the common pathway through which joint vulnerabilities (i.e. cartilage pathology, pathomechanics and neuromuscular control faults) are translated into pain and hand impairments – then, OA related pain and impairments may be mitigated by altering the physical activities that produce damaging joint forces (reducing the abnormal or excessive forces), and by improving the joint's capacity during physical activity to manage force.

Commonly, muscle strengthening and joint mobilization exercises are included in hand OA therapy. The view of OA as mechanically driven, primarily through physical activity, provides a rationale for also looking into the potential to improve clinical outcomes through the training of the neuromuscular and sensorimotor functions (i.e. proprioception, coordination), which help regulate joint movement and help protect the joint from injury. Therapeutic techniques for these purposes are available. What is not known, but can be tested at low risk to research participants, are the effects of change in these functions upon hand OA symptoms and clinical OA progression.

The dynamic, intra-articular forces on small hand joints are difficult to assess directly. We can, however, clinically assess and train physical activity (the hypothesized generator of the forces) and determine the effects of training on OA hand symptoms (the clinically meaningful consequences of the damaging force).

Joint protection training is one means for altering physical activity. Joint protection principles are intuitively sound, but general. Improving joint protection training specificity and potency may depend upon better understanding of the interactions between symptoms and physical activities, such as the types of physical activity (i.e. gripping, rotating, striking, vibrating, etc.), dimensions of physical activity (i.e. speed, repetition and duration) and performance conditions (i.e. mood, expectation for the activity and competence with the activity) that intensify or diminish OA symptoms.

Pain appears to be both message and messenger. Suppression of pain, although a priority, is only the first step in obtaining lasting relief from it. The different origins of pain (articular warning, inflammatory cascade and neurogenic pathology) may require different therapeutic strategies. Methods for identifying meaningful subgroups of hand pain are needed and would likely facilitate OA hand pain treatment planning.

The questions surrounding the issues of hand OA and physical activity as framed in this report lend themselves to an array of research approaches, observational and experimental, in particular, given the earlier stage of theory development, speculative nature and the complexity of the problems; grounded-theory methodologies, which incorporate in-depth study of the interactions among patient experience of OA-related symptoms, impairments and physical activities; action research models, which engage patients as active participants in the design and evaluation of the therapeutic interventions and processes; and single subject experimental trials that test treatment techniques and that can be summarized and meta-analysed to produce stable and generalizable results. ⁴⁷