The atrophic type of hip osteoarthritis (OA) is characterized by cartilage degradation without the formation of osteophytes. Individuals with atrophic OA have been less well studied, and it is unknown whether this OA type differs from the osteophytic types with regard to bone tissue. The purpose of this study was to examine bone mineral density (BMD), hip structural properties, and fracture risk in individuals with the atrophic type of OA as compared to those with the osteophytic types (normotrophic/hypertrophic) as well as individuals without OA.
This study is part of the Rotterdam Study, a large prospective population-based cohort study. We examined 5,006 participants who had been assessed for OA, BMD, and geometric measures at baseline and for incident nonvertebral osteoporotic fractures (mean followup 9.6 years). We estimated the differences in bone characteristics between the OA groups and the controls (no joint space narrowing or osteophytes). Cox proportional hazards regression was used to calculate osteoporotic fracture risk.
Participants with atrophic OA had systemically lower BMD as compared to those with normotrophic OA and as compared to the controls (6.5% and 9% for total body BMD; 4% and 5% for skull BMD, respectively). Participants with osteophytic OA had ∼4% and ∼5% higher total body and skull BMD, respectively, a wider femoral neck, and greater bone strength (12% and 5% higher section modulus, respectively) as compared to the controls or to those with atrophic OA. The risk of osteoporotic fractures was almost 50% higher in those with atrophic OA as compared to the controls (hazard risk 1.48, P = 0.008). This difference was not explained by differences in the BMD, number of falls, degree of disability, or use of corticosteroids.
Individuals with atrophic hip OA have an increased risk of osteoporotic fractures that is not fully explained by systemically lower BMD as compared to controls.
[Show abstract][Hide abstract] ABSTRACT: The possible association between osteoporosis and osteoarthritis represents an ongoing matter of debate. It was considered, for decades, that both diseases were mutually exclusive due to the anthropometric characteristics and the difference in bone mass that patients with osteoporosis and osteoarthritis often present. However, in recent years, it was pointed out that both processes can coexist, and even that they may have a direct relationship. In this paper we review some aspects of the association between both diseases from a temporal perspective.
[Show abstract][Hide abstract] ABSTRACT: Osteoporosis and related fractures disproportionately impact patients with advanced age, those with the frailty phenotype, and those with multiple comorbidities. Recent studies report a changing incidence in fracture type among the oldest old throughout the world, a finding not satisfactorily explained by advances in treatment of lifestyle factors. A growing recognition of the importance of muscle and bone interaction is leading to improved understanding of the underlying biochemical pathways linking them and new therapeutic targets. New models of care for frail older populations, particularly after hip fracture, are being developed but have been challenged to identify appropriate outcomes to target. An appreciation for the relationship between age-related comorbidities, fracture risk, and competing mortality risk is essential for practitioners caring for the oldest-old population.
Current Osteoporosis Reports 08/2013; 11(4). DOI:10.1007/s11914-013-0158-z
[Show abstract][Hide abstract] ABSTRACT: Osteoarthritis characterizes the joint disease that results in cartilage damage accompanied by bone lesions and synovial inflammation. Joint integrity results from physiological interactions between all these tissues. Local factors such as cytokines and growth factors regulate cartilage remodeling and metabolism as well as chondrocyte differentiation and survival. Tremendous progress has been made through the use of animal models and provided insight for the mechanism of cartilage loss and chondrocyte functions. Surgical, chemical or genetic models have been developed to investigate the role of molecules in the pathogenesis or treatment of osteoarthritis. Indeed, the animal models are helpful to investigate the cartilage changes in relation to changes in bone remodeling. Increased bone resorption occurs at early stage of the development of osteoarthritis, the inhibition of which prevents cartilage damage, confirming the role of bone factors in the crosstalk between both tissues. Among these numerous molecules, some participate in the imbalance in cartilage homeostasis and in the pathophysiology of osteoarthritis. These local factors are potential candidates for new drug targets.
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