Effect of systemic comorbidities on OA-phenotypes: hypercholesterolemia, gout, osteoporosis and hypothyroidism

Abstract

Osteoarthritis (OA) is characterized by loss of cartilage (joint space narrowing) and osteophytes. OA is not only a joint disorder associated with mechanical stress and aging but also a multifactorial disease in which several risk factors work together to contribute to disease initiation or progression. Higher BMD has been associated with OA, principally with a bone phenotype characterized by presence of osteophytes (hypertrophic form) and low bone mineral density/osteoporosis has been associated with a phenotype driven by loss of cartilage thickness (atrophic form) of OA. In addition to osteoporosis, there are other systemic comorbidities that might have influence in the phenotypic and clinical presentation of OA (cartilage loss and/or osteophytes, pain, disability). Gout, hypothyroidism and hypercholesterolemia have been previously associated with OA without a definite consensus regarding its influence on the clinical and phenotypic presentation of OA at several joints. High cholesterol levels in the body has been associated with higher body mass index (BMI) and OA initiation and subjects who are overweight or obese tend to develop hypercholesterolemia due to changes in fat metabolism. However, there is still a debate as to whether high cholesterol levels affect the incidence of OA. Epidemiologic studies have not been conclusive. In addition gout has been associated with OA. Individuals with gout had more severe knee OA as defined by higher Kellgren-Lawrence grades, poorer self-reported functional capabilities and increased bilateral involvement compared with hyperuricaemic or normouricaemic individuals. Monosodium urate (MSU) crystal deposition are typical effect of gouty inflammation and might be visualized on radiographs as calcification of articular cartilage. Besides, calcification of articular cartilage in the hip and knee joints is highly prevalent independent of age, but is associated with histological OA. Therefore, it is important to determine the phenotypic characteristics of the joints with gout and its clinical relevance. Finally, studies have identified a putative role for thyroid hormone metabolism in articular cartilage maintenance and the pathogenesis of osteoarthritis. However, there is not conclusive evidence about the phenotypic presentation of OA in patients with hypothyroidism. These diseases, hypercholesterolemia, gout, osteoporosis and hypothyroidism are prevalent chronic diseases among adults with OA and in general, elderly population. We analyzed data from 600 interviews to patients with hip and/or knee OA assisting to the orthopedic consult of the Hospital Sao Vicente de Jundiai-Brazil and we observed that hypercholesterolemia is present in 37%, hypothyroidism 10% and gout 7.4%. We would like to define the phenotypic presentation of OA in subjects affected for these diseases and to identify the effect of these comorbidities on pain and disability of this population affected with OA. (AU)