Shari Ling, M.D.

Aging Connective Tissue and Osteoarthritis
Richard F. Loeser, Jr. MD. Rush Medical College and Rush-Presbyterian-St. Lukes Medical Center, Chicaco IL

Scope of the problem: The graying of America brings with it an increasing proportion of older adults. Aging is the strongest risk factor for the development of OA. Dr. Loeser provided an introductory overview of aging connective tissue as a contributor to the development of osteoarthritis (OA) and addressed three related issues.

First, how aging relates to OA development: There are age-associated changes in cartilage, bone and muscle that increase the risk of injury and damage and decrease the capacity to repair the damage sustained. These changes are cellular (chondrocyte density and response to IGF) and structural (advanced glycation end-product accumulation). Although cartilage degeneration evolves as the result of failure to repair damage induced by degradative processes. Others have begun to explore the contributions important toperi-articular structures (bone and muscle) in disease development and progression.

Second, Dr. Loser reviewed how aging affects the evaluation of older adults with musculoskeletal complaints. The high prevalence of radiographic OA and autoantibodies may be misleading and represent an underlying challenge for clinicians who must distinguishing abnormalities that contribute to complaints from those that are incidental distractions. Furthermore, co-morbid impairments such as cognition or concomitant cardiovascular disease can compromise the reliability of historic information, or physical findings.

Third, how management of OA differs for older patients was reviewed. The management of OA in older adult patients is challenging because of cognitive impairment, the high prevalence of co-morbid illness, risk of polypharmacy and drug interactions. Hence the importance of non-medicinal interventions such as resistive or aerobic exercise training, use of orthotic devices and bracing, weight reduction for overweight and obesity, and psychosocial support were emphasized as effective means of reducing pain and disability, and improving function for older adults with OA. Finally, the possibility of altering progression of OA in older adult patients with exercise, biomechanical interventions, growth factors or MMP inhibitors, and nutritional interventions were addressed.

Several autoimmune diseases increase with advanced age: temporal arteritis, Hashimotos thyroiditis and Sjogrens syndrome. There is an increased prevalence of autoantibodies such as rheumatoid factor and anti-nuclear antibodies, and pro-inflammatory cytokines (IL-1, IL-6 and TNF-a) and chemokine function in older adult patients. These factors are thought to be related and are hypothesized to arise from age-associated reduced T-cell DNA methyltransferase activity and hypomethylation that results in T-cell LFA-1 overexpression and autoimmunity.

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