in the Japanese Dental Science Review is an interesting and unique paper comprehensively describing the classical and recent publications on the mandibular condylar cartilage, containing 98 references, covering a wide range from clinical Nivolumab supplier to biological studies [1]. Mandibular condylar cartilage is termed secondary cartilage because of its characteristic developmental process, emerging from the distal and lateral part of the mesenchymal cell aggregate (the anlage of mandibular condyle), apart from Meckel’s cartilage, and unites

with the anlage of the mandible (the mandibular ramus) [2]. In terms of the anatomical localization, the principal function of this cartilage is to provide a smooth lubricated surface for articulation and to facilitate the absorption and transmission of the mechanical load with a low frictional coefficient during jaw movement, i.e. chewing. In addition, a distinct feature of the mandibular condylar cartilage is to undergo endochondral ossification, regulated by pleitropic hormones, such as growth hormones, parathyroid hormone-related protein, basic fibroblast growth factor, and insulin-like growth factor-1 during

the developmental process [3] and [4], thereby serving as the growth center of the mandible, similar to the growth plate in the long bone. The mandibular condylar cartilage has characteristic features in its cellular components, extracellular matrix composition and degrading enzymes, and hormonal and mechanical regulation. PD0332991 chemical structure Generally, cartilage below tissue consists of a relatively small number of cells and an abundant extracellular matrix consisting of collagen types II, VI, IX, X, and XI and

aggrecan. For example, the growth plate cartilage of the long bone contains mostly type II collagen, while the mandibular condylar cartilage contains type I collagen, usually lacking in most cartilages. Reportedly, the mandibular condylar cartilage cells, but not the long bone cartilage cells, express cathepsin L, which degrades type I collagen and proteoglycan aggregates at low pH as well as collagen types II, IV, IX, and XI, even at pH values close to neutrality [5]. Further elucidation of these unique biological properties may clarify not only mandibular growth and development, but also help in developing new treatment strategies for deformities of the orofacial complex caused by impaired mandibular growth. “
“Periodontal diseases are the most common inflammatory diseases caused by plaque biofilm in the oral cavity. During the progression of periodontal diseases, the pathological change of gingivitis to periodontitis is characterized by the irreversible loss of tooth supporting apparatus, ultimately leading to the loss of the tooth. It includes the progressive destruction of whole periodontal tissue: the gingiva, periodontal ligament (PDL), cementum, and alveolar bone, as well as the connective tissue attachment between the root surface and alveolar bone [1].