Gordon G V, Villanueva T, Schumacher H R, Gohel V
J Rheumatol. 1984 Oct;11(5):681-6.
Inflammation has been suggested as a component in the osteoarthritic process. We have examined 150 knees at autopsy to correlate the degree of osteoarthritis (OA) with synovial inflammation, and with radiographic or pathologic evidence of calcification as a possible source of crystal induced inflammation. Roentgenographic evidence of calcification and histologic finding of synovial reaction (proliferation or inflammation) were seen more frequently (p less than .05) in the knees of patients with more advanced OA. Perichondrocytic staining for calcium and phosphorus was seen in 93% of patients with severe OA and in only 24% of those with normal or minimal OA. Calcium hydroxyapatite crystals were identified by electron microscopy in perichondrocytic and other areas in 8 of 15 cartilage samples with moderate to severe OA and in none with normal appearing cartilage. In advanced OA, there were bone fragments embedded in cartilage and synovium. Although the pathogenetic sequences are uncertain, we speculate that calcium hydroxyapatite (and pyrophosphate) crystals and/or bone shards can contribute to both synovitis and cartilage degeneration.
炎症被认为是骨关节炎进程中的一个组成部分。我们对150个膝关节进行了尸检,以关联骨关节炎(OA)的程度与滑膜炎症,以及与作为晶体诱导炎症可能来源的钙化的影像学或病理学证据。在OA更严重的患者膝关节中,钙化的X线证据和滑膜反应(增殖或炎症)的组织学发现更频繁出现(p<0.05)。在93%的重度OA患者中可见软骨细胞周围钙和磷染色,而在正常或轻度OA患者中仅24%可见。在15个中度至重度OA软骨样本中的8个样本中,通过电子显微镜在软骨细胞周围及其他区域鉴定出了羟基磷灰石晶体,而外观正常的软骨样本中未鉴定出。在晚期OA中,有骨碎片嵌入软骨和滑膜。尽管发病机制尚不确定,但我们推测羟基磷灰石(和焦磷酸盐)晶体和/或骨碎片可导致滑膜炎和软骨退变。