Incremental lines of von Ebner in dinosaurs and the assessment of tooth replacement rates using growth line counts

Dinosaur dentine exhibits growth lines that are tens of micrometers in width. These laminations are homologous to incremental lines of von Ebner found in extant mammal and crocodilian teeth (i.e., those of amniotes). The lines likely reflect daily dentine formation, and they were used to infer tooth development and replacement rates. In general, dinosaur tooth formation rates negatively correlated with tooth size. Theropod tooth replacement rates negatively correlated with tooth size, which was due to limitations in the dentine formation rates of their odontoblasts. Derived ceratopsian and hadrosaurian dinosaurs retained relatively rapid tooth replacement rates through ontogeny. The evolution of dental batteries in hadrosaurs and ceratopsians can be explained by dentine formation constraints and rapid tooth wear. In combination with counts of shed dinosaur teeth, tooth replacement rate data can be used to assess population demographics of Mesozoic ecosystems. Finally, it is of historic importance to note that Richard Owen appears to have been the first to observe incremental lines of von Ebner in dinosaurs more than 150 years ago.

Diverse roles of the tumor necrosis factor family member TRANCE in skeletal physiology revealed by TRANCE deficiency and partial rescue by a lymphocyte-expressed TRANCE transgene

Tumor necrosis factor-related, activation-induced cytokine (TRANCE), a tumor necrosis factor family member, mediates survival of dendritic cells in the immune system and is required for osteoclast differentiation and activation in the skeleton. We report the skeletal phenotype of TRANCE-deficient mice and its rescue by the TRANCE transgene specifically expressed in lymphocytes. TRANCE-deficient mice showed severe osteopetrosis, with no osteoclasts, marrow spaces, or tooth eruption, and exhibited profound growth retardation at several skeletal sites, including the limbs, skull, and vertebrae. These mice had marked chondrodysplasia, with thick, irregular growth plates and a relative increase in hypertrophic chondrocytes. Transgenic overexpression of TRANCE in lymphocytes of TRANCE-deficient mice rescued osteoclast development in two locations in growing long bones: excavation of marrow cavities permitting hematopoiesis in the marrow spaces, and remodeling of osteopetrotic woven bone in the shafts of long bones into histologically normal lamellar bone. However, osteoclasts in these mice failed to appear at the chondroosseous junction and the metaphyseal periosteum of long bones, nor were they present in tooth eruption pathways. These defects resulted in sclerotic metaphyses with persistence of club-shaped long bones and unerupted teeth, and the growth plate defects were largely unimproved by the TRANCE transgene. Thus, TRANCE-mediated regulation of the skeleton is complex, and impacts chondrocyte differentiation and osteoclast formation in a manner that likely requires local delivery of TRANCE.