title: Joint fluid from patients with failed total hip arthroplasty stimulates pit formation by mouse osteoclasts on dentin slices.
abstract: Periprosthetic bone resorption has been implicated in the failure of total joint arthroplasty. Osteolysis is reported to be associated with bone resorption induced by bone-resorbing cytokines, which are released from macrophages and fibroblasts in periprosthetic tissues after stimulation by wear debris generated in the joint cavity. Recent reports have suggested the concept of the effective joint space, which includes all periprosthetic regions that are accessible to joint fluid and wear debris. In this study, we examined the levels of interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), and tartrate-resistant acid phosphatase (TRAP) in joint fluid after failed total hip arthroplasty (THA) with osteolysis and investigated whether the joint fluid could activate osteoclastic bone resorption using unfractionated mouse bone cells cultured on dentin slices. Histochemical analysis showed the presence of more TRAP-positive cells in synovial capsules from failed THA patients when compared with osteoarthritis (OA) patients (controls). The levels of IL-6, sIL-6R, and TRAP in joint fluid from failed THA patients were significantly higher than in OA patients. Mouse osteoclasts cultured on dentin slices with joint fluid from failed THA patients with osteolysis produced a significant increase of pit area, whereas cells cultured with joint fluid from OA patients did not. Interestingly, osteoclastic bone resorption on dentin slices was significantly correlated with TRAP activity in joint fluid (p < 0.0001). These results suggest that joint fluid containing bone-resorbing cytokines is produced by synovial capsules in failed THA patients with osteolysis and may activate osteoclasts around the prosthesis in combination with those produced by interface tissues, thus contributing to periprosthetic bone resorption.
authors.affiliation: Department of Orthopaedic Surgery, Tokyo Women's Medical College, Japan.
authors.forename: K J
authors.initials: KJ
authors.lastname: Kim
authors.forename: H
authors.initials: H
authors.lastname: Hijikata
authors.forename: T
authors.initials: T
authors.lastname: Itoh
authors.forename: M
authors.initials: M
authors.lastname: Kumegawa
mesh_terms: D000135:Acid Phosphatase / Q000097:blood / Q000378:metabolism; D000818:Animals; D019644:Arthroplasty, Replacement, Hip; D001862:Bone Resorption; D003804:Dentin / Q000378:metabolism*; D006651:Histocytochemistry; D006801:Humans; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D007527:Isoenzymes / Q000097:blood / Q000378:metabolism; D051379:Mice; D010010:Osteoclasts / Q000502:physiology*; D019947:Receptors, Interleukin-6 / Q000097:blood / Q000378:metabolism; D013582:Synovial Fluid / Q000201:enzymology / Q000378:metabolism / Q000502:physiology*; D000071681:Tartrate-Resistant Acid Phosphatase; D017211:Treatment Failure
chemical_list: D015850:Interleukin-6; D007527:Isoenzymes; D019947:Receptors, Interleukin-6; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase