Abstract
The formation of mineralized deposits in human articular cartilage is a common occurrence [1–4]; however, the relationship between mineral deposition and material properties of the articular cartilage is not well understood nor the relationship between mineral deposition and the development of degenerative joint disease. Several different crystalline structures have been identified in articular cartilage and synovial fluid including monosodium urate, calcium pyrophosphate dihydrate (CPPD), and basic calcium phosphates (BCPs). These distinct mineral phases are associated with specific pathologies and mechanisms of crystal formation such as the development of monosodium urate in gout and CPPD in pseudogout. Less is known regarding the deposition of BCPs, a class of compounds including carbonate-substituted hydroxyapatite (cHA), tricalcium phosphates (TCP), octacalcium phosphate (OCP), and whitlockite, in articular cartilage. The presence of BCP calcification of articular cartilage in humans has been associated with decreased joint function [1, 3], aging [2] and severity of osteoarthritis [1, 3]. Commonly used methods of crystal detection such as polarized light microscopy of synovial fluid and conventional radiography of the joint can be insensitive to the detection of BCP crystals and more sensitive techniques such as microradiography or electron microscopy of articular cartilage sections are required to detect areas of BCP mineralization [3, 5, 6]. It is not yet known how regions of mineralization may influence the tribological properties (friction, wear, and lubrication) of the articulating surfaces and the material and structural properties of articular cartilage. Animal models with which to study the mechanisms of mineralization of articular cartilage are limited.
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