Osteoarthritis☆
Introduction
Osteoarthritis (OA), the most common joint disease, is among the most frequent and symptomatic health problems for middle aged and older people [1], [2], [3], [4], [5], [6], [7]. It is characterized by joint pain and dysfunction; and, in its advanced stages, joint contractures, muscle atrophy and limb deformity [8], [9], [10]. OA is caused by joint degeneration, a process that includes progressive loss of articular cartilage accompanied by attempted repair of articular cartilage, remodeling and sclerosis of subchondral bone, and osteophyte formation [9], [10]. Although increasing age and excessive articular surface contact stress increase the risk of degeneration in all joints, the pathophysiology of the joint degeneration that leads to the clinical syndrome of OA remains poorly understood. For this reason, efforts to prevent this disease or slow its progression are based more on speculation than science. Current treatments do not prevent or cure OA, and symptomatic treatments often fail to provide satisfactory pain relief. Once patients develop OA, they suffer from the disease for the remainder of their lives and the severity of pain and disability generally increase. The frequency and chronicity of OA and the lack of effective preventive measures or cures make this disease a substantial economic burden for patients, health care systems, businesses, and nations [2], [3], [5], [6], [11], [12], [13], [14].
Improving the prevention and treatment of OA will require finding methods of preventing and slowing the joint degeneration that causes OA and decreasing the joint pain and dysfunction. This manuscript was developed in part from the authors' previously published works [8], [9], [15], [16], [17], [18], [19]. It examines the clinical classification, incidence, prevalence, costs, distribution among joints, risk factors, and natural history of OA. The final section discusses approaches to restoring degenerated joint surfaces.
Section snippets
Diagnosis
Osteoarthritis results from degeneration of a synovial joint: a generally progressive loss of articular cartilage accompanied by attempted repair of articular cartilage, remodeling and sclerosis of subchondral bone, and in many instances the formation of subchondral bone cysts and marginal osteophytes [8], [9]. In addition to the changes in the synovial joint, usually demonstrated by plain radiographs, diagnosis of the clinical syndrome of osteoarthritis requires the presence of chronic joint
Classification
OA develops most commonly in the absence of a known cause of joint degeneration, a condition referred to as primary or idiopathic OA [9], [10]. Less frequently, it develops as a result of joint degeneration caused by injuries or a variety of hereditary, inflammatory, or developmental, metabolic, and neurologic disorders, a group of conditions referred to as secondary OA (Table 1) [9], [10]. Idiopathic OA rarely occurs in people younger than 40 years. Secondary OA, caused by joint insults or
Prevalence, incidence, and costs
To some extent, estimates of the prevalence, incidence and costs of OA depend on the criteria used to diagnose the disorder. Symptoms of persistent joint pain and stiffness and evidence of joint degeneration, typically radiographic evidence of articular cartilage loss, osteophytes, and in some instances increased subchondral bone density and cysts, establish the diagnosis of OA [8]. More severe joint degeneration is associated with increased prevalence of pain, but the prevalence of pain
Distribution among joints
Osteoarthritis can affect any synovial joint. Idiopathic OA rarely occurs in the ankle, wrist, elbow and shoulder, but it is common in the hand, foot, knee, spine and hip joints [5], [6], [21], [22], [27], [31], [39] In a study of 607 consecutive patients referred to the University of Iowa orthopaedic clinic for treatment of severe ankle, hip or knee OA, 7% of the patients with ankle OA, 69% of the patients with hip OA and 85% of the patients with knee OA had primary disease. Seventy-three
Risk factors
In addition to the disorders associated with the multiple forms of secondary OA (Table 1), genetic predisposition, obesity, female gender, greater bone density, and joint laxity have been identified as risk factors [21], [57], [58], [59], [60], [61]. Although these factors may increase the risk of OA in selected populations, the most important risk factor in all populations is age. Mechanical loading that exceeds the ability of a joint to repair or maintain itself is another universal risk
Natural history
Although physicians and patients commonly regard OA as relentlessly progressive, [62] the disease does not necessarily follow this course (Table 2) [89], [120], [121], [122], [123], [124], [125], [126], [127], [128]. The symptoms of OA may remain unchanged, slowly progress over many years, improve temporarily, or progress rapidly to the point that the patient is disabled within a few years of the onset of the disease [20], [39]. Most patients with OA have intervals of symptomatic improvement [9]
Restoring degenerated articular surfaces
For more than 250 years surgeons have been seeking ways to repair or regenerate degenerated articular surfaces. Repair refers to restoring a damaged articular surface with new tissue that resembles but does not duplicate the structure, composition and function of articular cartilage; regeneration refers to forming new tissue indistinguishable from normal articular cartilage [17], [130], [131], [132]. They made little progress for 200 years, but in the last 50 years use of surgical procedures to
Conclusions
Despite the great success of joint replacement and the proliferation of medical, nutritional, and physical treatments, the problem of OA has not been solved, and its adverse impacts on individuals, populations and economies will continue to increase. Replacing a severely degenerated joint with an implant is much like replacing a failing heart with a mechanical pump, both operations restore function, but neither treats the disease, the costs are high and the complications severe. None of the
Acknowledgement
The work reported in this manuscript was supported by award P50 AR48939 National Institutes of Health Specialized Center on Research for OA. http://poppy.obrl.uiowa.edu/Specialized Center of Research/SCOR.htm. This grant was awarded to the University of Iowa and the authors receive salary and research support from the grant.
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This review is part of the Advanced Drug Delivery Reviews theme issue on “Drug Delivery in Degenerative Joint Disease”, Vol. 58/2, 2006.