The Identification of CD163 Expressing Phagocytic Chondrocytes in Joint Cartilage and Its Novel Scavenger Role in Cartilage Degradation

Abstract

BackgroundCartilage degradation is a typical characteristic of arthritis. This study examined whether there was a subset of phagocytic chondrocytes that expressed the specific macrophage marker, CD163, and investigated their role in cartilage degradation.MethodsCartilage from the knee and temporomandibular joints of Sprague-Dawley rats was harvested. Cartilage degradation was experimentally-induced in rat temporomandibular joints, using published biomechanical dental methods. The expression levels of CD163 and inflammatory factors within cartilage, and the ability of CD163+ chondrocytes to conduct phagocytosis were investigated. Cartilage from the knees of patients with osteoarthritis and normal cartilage from knee amputations was also investigated.ResultsIn the experimentally-induced degrading cartilage from temporomandibular joints, phagocytes were capable of engulfing neighboring apoptotic and necrotic cells, and the levels of CD163, TNF-α and MMPs were all increased (P<0.05). However, the levels of ACP-1, NO and ROS, which relate to cellular digestion capability were unchanged (P>0.05). CD163+ chondrocytes were found in the cartilage mid-zone of temporomandibular joints and knee from healthy, three-week old rats. Furthermore, an increased number of CD163+ chondrocytes with enhanced phagocytic activity were present in Col-II+ chondrocytes isolated from the degraded cartilage of temporomandibular joints in the eight-week experimental group compared with their age-matched controls. Increased number with enhanced phagocytic activity of CD163+ chondrocytes were also found in isolated Col-II+ chondrocytes stimulated with TNF-α (P<0.05). Mid-zone distribution of CD163+ cells accompanied with increased expression of CD163 and TNF-α were further confirmed in the isolated Col-II+ chondrocytes from the knee cartilage of human patients with osteoarthritis, in contrast to the controls (both P<0.05).ConclusionsAn increased number of CD163+ chondrocytes with enhanced phagocytic activity were discovered within degraded joint cartilage, indicating a role in eliminating degraded tissues. Targeting these cells provides a new strategy for the treatment of arthritis.

Reducing dietary loading decreases mouse temporomandibular joint degradation induced by anterior crossbite prosthesis

“…It has been reported that although the soft diet plays a negative role in condyle development 5,9,10 , rabbits or rats that received TMJ discectomy had less degenerative cartilage changes 43,44 and higher condylar cartilage sulfate uptake 45 when fed with soft diet. Besides catabolic changes, the chondrocytes in mechanically induced degraded articular cartilage displayed the reparative capability, including the activities of phagocytizing dead cells 46 and proliferation 26,33,36,37 . Hence, there might be a stronger repair response in TMJ cartilage in the small-size diet than the large-size diet group while the mice received the same kind of abnormal prosthesis.…”

Connexin43 hemichannels mediate small molecule exchange between chondrocytes and matrix in biomechanically-stimulated temporomandibular joint cartilage

“…Primary rat chondrocytes were isolated as described previously [40]. In brief, chondrocytes were isolated from the condylar cartilage of 3-week-old female rat TMJs by digestion with 0.25% trypsin (Hyclone, Logan, UT, USA) for 20 min, followed by digestion with 0.2% type II collagenase (Invitrogen) for 2 h. Chondrocytes were resuspended in Dulbecco’s modified Eagle’s medium (DMEM, Hyclone) containing 10% fetal bovine serum (Hyclone) and then cultured in a fully humidified atmosphere with 5% CO 2 at 37°C for 3 days before use.…”

Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

“…Some have proposed that, having isolated chondrocytes from degenerated rat cartilage, that phagocytosis could be handled by chondrocytes displaying a dedicated phenotype (i.e., type II collagen + /CD163 + ), in which phagocytic activity was measured, suggesting a role in the clearance of apoptotic and necrotic cells [103]. Hashimoto and coworkers demonstrated that apoptotic bodies derived from chondrocytes, treated with sodium nitroprusside (SNP) or anti-Fas, contained both nucleotide pyrophosphohydrolase (NTPPH) and alkaline phosphatase activities and could precipitate Ca ++ [104].…”