CPPD and Associated Crystals in Clinically Diagnosed Chondrocalcinosis: A Clinicopathological Study of 20 Patients

Abstract

Introduction: Chondrocalcinosis (Ch-C), induced by calcium pyrophosphate dihydrate crystals (CPPD) [Ca2P2O7.2H2O] is considered as a distinct metabolic disease and a well-defined clinical entity, with characteristic clinical manifestations and symptoms. This study used previously found method by the author .i.e, non-staining approach to discover crystal deposits in patients with clinically diagnosed Ch-C, to find a possible correlation between coexisting crystals, and to assess the role of coexistent crystals in inflammatory cellular processes of joints. Patients and methods: There were forty (40) surgical specimens that had been traditionally processed from 16 patients who had been clinically diagnosed with Ch-C. Results: In unstained tissue sections CPPD crystals were found in 22 of 40 samples of all 16 patients. Beside the CPPD crystals calcium hydroxyapatite (HA) [Ca5(PO4)3(OH)] crystals were found in 26 tissue samples of all 16 patients, cholesterol (CC) [C27H46O] in 23 tissue samples of 12 patients, and crystalline liquid lipid droplets (CL) in 11 tissue samples of 5 patients. More or less amorphous deposits of calcium carbonate [CaCO3] and/or calcium phosphate [Ca3(PO4)2] were present alongside CPPD and the contemporaneous crystals. There was a significant and positive correlation between prevalence of CPPD and HA. The connection between inflammatory cellular infiltration and CPPD, HA, CC or CL crystals surrounded by mineral deposits was not significant. Conclusions: The non-staining approach is a practical, low-tech way to find CPPD, HA, CC, and other crystals (with or without CL). The positive and significant correlation between CPPD and HA support the earlier premise that CPPD and HA represent basically an identical metabolic disorder). CPPD and/or HA crystals can provoke inflammatory processes responsible for the clinical symptoms, but the variable amounts of amorphous minerals enclose (isolate) the crystals, and can reduce or eliminate the inflammatory reaction. The authors assume that CC (with or without CL) is an associated phenomenon (concomitant fat metabolic malady) without direct cause of inflammation, and is not responsible for clinical symptoms of crystal induced arthropathies.