This model of osteoarthritis appears to be well established in the scientific community and is accepted by most physiotherapists and by many osteopaths and osteopathic physicians. However, dissenting opinions continue among clinicians.^5-8 Why do some elderly individuals experience no joint pain at all and display no other signs of deterioration apart from some joint space narrowing? Why, if osteoarthritis follows a purely age-related model, is there an accelerated deterioration process after trauma—even in young people, especially if the trauma affects intraarticular structures? Considering that particular occupations and sports activities produce focal and predictable osteoarthritic problems, indicating a strong “wear-and-tear” mechanism, how important is that mechanism in general presentations? With good evidence that usage and trauma play dominant roles in premature osteoarthritis, are the study participants in any cohort merely age candidates, or have they actually accumulated specific degradations? 

The hereditary or genetic links for osteoarthritis are also problematic. The familial mechanism for this condition was first identified more than 60 years ago in studies of Heberden's nodes.⁹ Generations of women in New Zealand have presented with Heberden's and Bouchard's nodes on their second and third digits from darning, sewing, embroidery, and knitting, though personal observation suggests that these nodes are becoming less common as fewer women engage in these activities. Thus, the transfer of habit and skills from mother to daughter produced a predictable familial association, but this association was occupational rather than genetic in nature. Other familial patterns, such as structural femoral and carrying angles in mothers and daughters, may also increase the likelihood of osteoarthritis. Earlier this year, a review¹⁰ concluded that chromosomal associations in patients with osteoarthritis are numerous but unspecific, and despite much effort, researchers have been unable “to reach a genuine therapeutic target or even a prognostic marker of [osteo arthritis].” 

Nutrition and tribologic issues are key in development of osteoarthritis. Being mostly avascular, articular cartilage is largely supported by diffusion. Articular margins receive nutrients from the adjacent vascular synovium and periosteum.¹¹ Deeper layers of articular cartilage may be fed by the blood supply to the subchondral bone, but this mechanism is less clear. The deep cartilage layers are not subject to the shear forces sustained by the superficial layer, and the deepest layer is reported to be largely calcified.¹¹ 

The contacting surfaces in joints are pivotal in the deterioration process. Although the diffusion that the tangential zone experiences from below is contested, synovial fluid intake from the joint cavity is well established as a predominant mechanism.¹² Absorption from the surface appears to be largely osmotic, possibly assisted by a mechanical pump phenomenon, though such a process is now disputed.¹² Surface cartilage is normally more hydrated than interior layers because the presence of proteoglycans on the surface allows binding of water molecules, which are exuded under compression (ie, “weeping lubrication”).¹³ 

Since the work of McCutchen¹⁴ in the 1960s, the understanding of lubrication in human joints has been considerably refined. However, there are still a number of proposed mechanisms of joint lubrication under investigation,¹⁵ and the complexities of transient, cyclic, and prolonged loadings are becoming increasingly apparent.^12,16-18 

Furey¹⁸ has stressed that friction, lubrication, and wear are each separate issues in osteoarthritis, and abrasive forces are accompanied by delaminatory stresses and other subsurface stresses. Whatever tribologic model is followed, the pressure of the surfaces is a key factor. Increased surface pressure not only increases abrasive and shear forces and decreases lubrication, but it also adversely affects transport of nutrients and waste products if sustained. Although immobilized joints undergo atrophy of articular cartilage, presumably because they lack boosted or pumping lubrication, joints exposed to prolonged compression can also undergo atrophic changes.¹¹ Therefore, the effectiveness of the mechanical integrity of surface cartilage in resisting tribologic stress may be as important as nutrition and lubrication in joint deterioration.¹⁹ 

In the tangential zone, collagen is aligned parallel to the surface, providing improved shear resistance compared with vertical or oblique arrangements. Collagen fibers run obliquely to each other in tight bundles, forming a strong matting that has multidirectional resistance to shear. External to the joint, ligamentous competency is important for mechanical integrity, providing constraints to undue displacement (especially in close-packed situations) so that joint congruency is preserved. 

Less well understood is how the “choreography” of muscles around a healthy joint controls the ratio between rolling and gliding motions. Rolling action involves less shear stress on the contact surfaces, and joint lubrication mechanisms are enhanced by rolling. Research published on the kinematic characteristics of the knee show the importance of muscular control,²⁰ but the classic example of muscular choreography involves the glenohumeral joint, in which stability is only partly established by the labrum.²¹ As the arm makes complex arcs of movement, any derangement of muscular coordination leads to painful impingement syndromes (eg, frozen shoulder, painful arc syndrome, supraspinatus bursitis). Even in saddle joints and so-called gliding joints, articulation may be more rolling than gliding if the muscular and ligamentous systems are functioning optimally. 

Most studies considering laterality associations in osteoarthritis have found incidence bias. In the Johnston County Osteoarthritis Project,²² which examined multijoint presentations, a strong association was found between contralateral knee and hip pairs, and a modest association was found with the other joint site (ie, knees vs hips). Although these findings appear to support the age-oriented model of osteoarthritis, it is more likely that compensatory gaits and the use of gait aids, such as canes and walkers, greatly increase stresses on other joints if there is restriction in a joint system. This process starts well before radiographic signs of joint degradation are visible. 

Newton and Seagroatt²³ suggested that differences they observed in osteoarthritis rates between the right and left hips (average rates: 60% right, 40% left) in 4 surveys of osteoarthritis and arthroplasty (2 from England and 2 from other countries) were caused by higher impulse loading in right-footed patients. In a survey of data in Italy, Stea et al²⁴ observed an overall bias toward right hip arthroplasty (rate, 58%), but a higher prevalence of right hip osteoarthritis in left-footed patients. Right-footed individuals were unbiased for monolateral arthroplasty (average rates: 50.7% right, 49.3% left), but left-footed individuals exhibited a strong differential toward arthroplasty on the right side (average rates: 76.8% right, 23.2% left). Stea et al²⁴ concluded that left-footed patients subjected their right sides to greater stress than right-footed patients. 

Stea et al²⁴ supported their conclusions with a general population survey that found that left hips had slightly more loss of initial joint space in right-footed people than in left-footed people. The authors explained this survey finding as being the result of either intrinsic differences between right and left hips or of the left hip being subjected to greater mechanical stresses in right-footed people. They also postulated that early cartilage loss may target the left hip, but after a threshold is reached, joint deterioration might progress more symmetrically. 

Without elaborating on the complex body patterning associated with left and right dominance, it is important to note that the conclusions of the Johnston County Osteoarthritis Project,²² Newton and Seagroatt,²³ and Stea et al²⁴ do not necessarily contradict each other. Each study supports dominance usage as a factor in osteoarthritis development. 

In a prospective multicenter cohort study in the United Kingdom, Birrell et al²⁵ considered laterality in primary care assessments of new hip pain in 195 patients who were assessed and then tracked until referral for total hip arthroplasty. Importantly, less compensatory stresses on other joints were present during the initial assessments. This cohort displayed initial bias toward right hip pain (rates: 53% right, 45% left), with only 5 of the 195 patients exhibiting bilateral pain initially.²⁵ 

The ratios in all these studies correlate with laterality ratios for various joint replacement procedures recorded in the New Zealand National Joint Register (S. Shaw, PhD, written communication, December 2010). These data, shown in the Table, also indicate a greater spread in laterality ratios for the upper extremities, where usage bias is greater. 

Such laterality bias in osteoarthritis serves as a strong argument for a usage-based model of the condition, especially when added to occupational, ergonomic, and sports evidence. In the age-only model of osteoarthritis, by contrast, an explanation has yet to be established for laterality bias of the preliminary arthrosis stage. 

More fundamentally, the study by Birrell et al²⁵ shows that patients with pain scores between 3 and 7 (median, 5) on the visual analog scale, which ranges from 0 (no pain) to 10 (agonizing pain), already have their hip flexion reduced to a range of 84° to 110°, with a mean of 98°. This dramatic reduction in hip flexion means that in most sitting situations (eg, on soft furniture; in cars, planes, or the cinema), there is maximum capsular torsion. Even in sitting positions that approximate 90°, such as during dining and elimination, the joint cartilage will be in prolonged compression. With increasingly sedentary lifestyles, this is an important etiologic consideration. 

Garbuz et al³⁸ found that waiting time for surgery was strongly associated with reduced outcome scores after total hip arthroplasty, with an 8% average reduction in outcome score with every additional month of waiting. The worst outcomes occurred in patients who had more pain, lower function, and more hip stiffness preoperatively. Other researchers have found strong associations between postoperative outcome and preoperative walking time and hip flexion arc. Patients with worse preoperative scores in these categories had greater likelihood of postoperative pain and lower functional outcomes.^39,40 These results support the hypothesis that joint degradation accelerates dramatically after the arthritis phase is reached. 

There are substantial clinical implications in this proposed alteration of the osteoarthritis model (Figure). In this revised model, osteoarthritis is not an inevitable disease of aging but the result of a definable history in the individual. Age-related changes do not lead to osteoarthritis by themselves. Rather, there must be some additional stress or insult to cause the condition. The greatest risk factor for osteoarthritis is not age but duration and intensity of stressing. Obviously, family members will have similar pain-related biochemical characteristics, similar susceptibilities to mechanical and histologic breakdown, and similar inflammatory and immunologic responses. Nevertheless, osteoarthritis—first and foremost—depends on the individual's own history. 

Another implication is that joint restriction is causal rather than symptomatic, with restriction around the joint associated with early changes in the joint rather than late-stage degeneration. 

Furthermore, the altered model implies a reversible arthrosis phase before the irreversible arthritis phase. The traditional model maintains that osteoarthritis cannot be prevented or arrested, let alone reversed. Yet recent in vivo research using hydropolymers as scaffolding for chondrocyte seeding and cartilage regeneration shows that, given some relief from compression and shear, chondrocyte activity may be recoverable.⁴¹ This finding bodes well for joint rehabilitation in the absence of subchondral exposure, as well as for manual therapy aimed at improving capsular freedom. 

Treatment intervention points are earlier. Preserving joint mobility offers the possibility of arresting further degradation, especially in earlier phases of osteoarthritis. Therefore, intervention points and goals of physical therapy are altered dramatically. As soon as maintenance pain relief is required in joint-related presentations, physical therapy should be introduced, combined with a program of effective stretching. Post-trauma and postsurgery rehabilitation needs to be immediate, comprehensive, and aimed at restoring articular freedom as well as limb function. 

Finally, some therapeutic interventions used for patients with osteoarthritis need to be reconsidered. Many resistance and weight-loaded exercises (including outdoor walking, treadmill sessions, and exercycles) involve short-arc repetitive motion, which tends to decrease joint mobility for the same reasons involved in repetitive occupational⁴² and sporting activities.⁴³ Physical therapy has traditionally concentrated on countering muscle strength imbalance in the agonist muscles around an affected joint system⁴⁴ by strengthening weak muscles and lengthening strong muscles. However, there is evidence that such muscular imbalance can originate from disturbance of joint proprioception,⁴⁵ and it is likely that short-arc exercise programs cause shortening of muscle action and place further stress on the joint capsule and joint surfaces. 

Although exercise of this type may improve congruency, such exercise is contraindicated in many cases, especially those cases involving joints that do not bear weight, such as the shoulder joint. Sustained static stretching of strong muscles, which also improves congruency, together with range-of-motion exercises are the preferred remedial choices for patients in these situations. Low-resistance loaded exercise would be the treatment of choice in early-stage hypermobile situations. For weight-bearing joints, low-resistance exercises such as aquaerobics, aquajogging, and swimming have a supportive role for patients who are obese, who have comorbid conditions, or who are elderly with sarcopenia.⁴⁶ 

Although there has been recent criticism of primary care physicians for neglecting weight-reduction and exercise programs⁴⁷ in managing osteoarthritis, most current exercise regimens tend to produce varied results for the previously mentioned reasons. In my experience, managing osteoarthritis in patients with comorbid obesity is a major clinical challenge that requires a carefully planned and multifaceted approach, even in early stages. While aerobic exercise is vital, the factors discussed in the present article need to be taken into account, often making tailoring of specific exercises necessary. The case for preventive management is therefore strong. 

Strapping may palliate pain simply by restricting movement, but it does not alleviate contact pressure, and it introduces novel congruency patterns.⁸ Lack of movement also promotes cartilage atrophy.¹¹ Strapping may retain a niche treatment role in hypermobile presentations, but its drawbacks limit its usefulness. In hypermobile presentations of osteoarthritis, as indicated by the Johnston County Osteoarthritis Project²² and the Italian study by Stea et al,²⁴ contralateral transfer of stress must be considered, and bilateral evaluation should be routine. Restriction in 1 joint system, such as the hip, transfers stress to other joint systems that are functionally linked and more mobile, such as the knee, as noted in the Johnston County study.²² The shoulder is similarly linked to grip, wrist, and forearm function. In addition, walking aids transfer stresses to other joint systems as the user assumes a flexed stance, producing additional problems in long-term use. 

In the arthrosis phase of osteoarthritis, manual therapy should target joint range, congruency, and periarticular muscle coordination to reduce contact (ie, capsular) pressure and surface friction. After the arthritis phase has been reached, manual therapy becomes palliative at best. Although it is difficult to determine the cut-off point for effectiveness of conservative manual therapy in remedying the problem, a useful clinical measure is that improvements in range of motion do not last between treatment sessions, and overall improvement reaches a plateau. From that point on, delaying surgery produces higher ancillary costs and worse outcomes.^38-40 

This revised model of osteoarthritis allows for the possibility that primary osteoarthritis might be preventable with improved body maintenance. Some of the costs of surgical interventions could be usefully transferred to government information programs highlighting stretching and mobility as important aspects of public health. The effectiveness of such information programs could be enhanced by conducting simple screenings (eg, supine hip flexion) and manual interventions (eg, facilitated positional release, muscle energy, strain-counter-strain) based on an improved understanding of the processes involved in joint degradation. 

As physicians and other healthcare providers manage populations that are not only growing older and increasing in BMI, but also becoming more sedentary, policymakers face the “perfect storm.” On the basis of arthroplasty projections for the United States,⁴⁸ primary hip replacements are expected to increase by 174% and knee replacements by 673% by 2030. The prevailing model of osteoarthritis does not correlate well with clinical experience, and it is hindering progress in improving these arthroplasty statistics. A new osteoarthritis model is overdue.