Prosthetic synovitis.
The term "prosthetic synovitis" is applied to reactive changes resulting from a synovial-like membrane formed between a failed prosthesis (noninfected) and the bone interface. This report is the result of light-microscopic and clinical examination of more than 100 specimens obtained at surgery of failed previous hip replacements. The morphology and cell distribution of those tissues removed at surgery in 51 noninfected cemented total hip operations allowed a quantitative estimate of surface cell population by a "touch imprint" technique; qualitative and quantitative estimate (scale, 1 to 4+) of cell population and foreign body materials by light microscopy; and electron microscopy and biochemical analysis of selected samples. Histologic examination included the following cell population, in decreasing order of frequency: acidophilic histiocytes (95%); giant cells (80%); fibronoid material (80%); lymphocyte and plasma cells (26%); and neutrophils (8%). Microscopic examination showed that the largest particles of acrylic cement and shards of high-density polyethylene appeared to be walled off by connective tissue capsules. The majority of smaller particles were incorporated into the histiocyte/macrophage or giant cell population. Histochemistry indicated that these particles elicited "foci" of cellular activity within the synovial-like membrane. This increased activity included the appearance of increased endogenous peroxidase activity in those macrophages within the "foci"; increased betagalactosidae activity among these histiocytes; and a localization of acid phosphates activity within giant cells along the borders of inclusions within the cell cytoplasm. We conclude that wear products resulting from total hip arthroplasty, including the bone cement, can induce increased lysosomal and proteolytic activity within the histiocyte and giant cell populations. It may be important to emphasize that there were "reactive foci" within the membrane and that the entire membrane, even though infiltrated with macrophages, did not respond uniformly to the presence of prosthetic debris. We advance a theory that the first step toward a distractive phenomenon at the interface is micromotion between the cement and bone. Micromotion may be caused by removal of subchondral plate during total hip replacement, leading to fatigue and loss of trabeculae and resultant increase motion, thus bone loss. Bone loss may be the direct result of mechanical injury, increased osteoclasis, or direct lysis of bone by various enzymes released by the interface membrane.
D000077:Acetabulum / Q000473:pathology; D001672:Biocompatible Materials; D001843:Bone Cements / Q000009:adverse effects*; D005269:Femur / Q000473:pathology; D005549:Foreign-Body Reaction / Q000209:etiology* / Q000473:pathology; D006615:Hip / Q000473:pathology*; D006622:Hip Prosthesis / Q000009:adverse effects*; D006644:Histiocytes / Q000473:pathology; D006801:Humans; D008768:Methylmethacrylates / Q000009:adverse effects; D010010:Osteoclasts / Q000473:pathology; D010544:Peroxidases / Q000032:analysis; D011095:Polyethylenes / Q000009:adverse effects; D011475:Prosthesis Failure; D013585:Synovitis / Q000209:etiology* / Q000473:pathology; D001616:beta-Galactosidase / Q000032:analysis
D001672:Biocompatible Materials; D001843:Bone Cements; D008768:Methylmethacrylates; D011095:Polyethylenes; D010544:Peroxidases; D001616:beta-Galactosidase