Arthritis & Rheumatism, Volume 63,
November 2011 Abstract Supplement
Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Chicago, Illinois November 4-9, 2011.
Adipokine Expression in Osteoarthritis Osteophytes.
Junker1, Susann, Frommer1, Klaus, Krumbholz1, Grit, Lehr2, Angela, Rehart2, Stefan, Rickert3, Markus, Steinmeyer3, Jürgen
Justus-Liebig-University of Gieben, Bad Nauheim, Germany
Markus-Hospital, Frankfurt, Germany
University Hospital Gieben and Marburg, Gieben, Germany
University of Erlangen-Nuremberg, Erlangen, Germany
Obesity is a recognized risk factor in osteoarthritis (OA) but little is known about the interaction between adipose tissue derived factors and bone formation. Adipocytes produce a variety of cytokine-like proteins, such as adiponectin, visfatin or resistin. While it is known that these adipokines are associated with the pathogenesis of rheumatoid arthritis and can be produced by other cell types such as fibroblasts, osteoblasts and osteoclasts, their role in osteophyte formation in OA has not been studied. Despite the mostly unknown mechanisms of osteophyte formation, there is growing evidence that inflammation and local stress contribute to this process. In this study, the expression of adipokines in osteophytes and their co-localization with cells of bone remodeling was analyzed.
Osteophyte tissue and cartilage was obtained from OA patients during joint replacement surgery. Serial sections of decalcified and deparaffinized osteophyte tissue were prepared. For histological overview, hematoxylin/eosin and Masson trichrome stainings were performed. Using these stainings, the osteophytes were scored and divided into grade one (early, small osteophyte, no ossification) to four (ossified osteophyte with cartilage). Immunohistochemistry was performed to identify sites and localization of adipokines using antibodies against alkaline phosphatase, vimentin, collagen type I, type II, adiponectin, visfatin, and resistin. TRAP stainings were performed to identify osteoclasts. Immunoassay analyses for visfatin were done with cartilage and isolated primary chondrocyte lysates.
Adiponectin, visfatin and resistin were detectable in all osteophytes of OA patients (grade 14). Adiponectin was localized around blood vessels as well as in some fibroblasts in the connective tissue of non-ossified osteophytes (25% of fibroblasts). In ossified osteophytes (grade 23), resistin and visfatin showed a co-localization with osteoblasts at the border of newly formed, non-mineralized bone tissue and with osteoblasts and osteoclasts at sites of bone resorption. In osteophytes without ossification (no detectable osteoblasts and osteoclasts, grade 1), visfatin and resistin were detectable only in single cells. Quantitatively, more visfatin than resistin expressing cells could be observed (resistin: 10% vs. visfatin: 25% of cells). ELISA using chondrocytes and cartilage confirmed the visfatin expression in these cells on the protein level.
The co-localization of visfatin and resistin with osteoblasts and osteoclasts in advanced osteophyte formation (grade 23) suggests that they may be involved in bone neo-formation and remodeling of OA osteophytes. In contrast, adiponectin was lower in advanced stages of osteophyte formation (grade 23) but present in early osteophytes that mainly consist of connective tissue (grade 1). These results indicate that visfatin, resistin and adiponectin may be involved in osteophyte formation at different stages and most likely affect different cell types of cartilage and bone formation during these processes.
Funded by the the ANCYLOSS project of the German Ministry of Research and Education (BMBF).
To cite this abstract, please use the following information:
Junker, Susann, Frommer, Klaus, Krumbholz, Grit, Lehr, Angela, Rehart, Stefan, Rickert, Markus, et al; Adipokine Expression in Osteoarthritis Osteophytes. [abstract]. Arthritis Rheum 2011;63 Suppl 10 :1825