A. R. Ten Cate

The role of fibroblasts in the remodeling of periodontal ligament during physiologic tooth movement.

Our findings indicate a cellular basis for the connective tissue remodeling which takes place during physiologic tooth movement. This cell is the fibroblast which is capable of synthesizing and degrading collagen simultaneously and, utilizing this ability, the orderly control of collagen remodeling within the periodontal ligament is possible. It is suggested that this cellular basis of connective remodeling will have a direct significance for orthodontic tooth movement once control mechanisms have been established.

The epithelial cell rests of Malassez and the genesis of the dental cyst

Abstract Activation of the epithelial cell rests of Malassez, both in vivo and in vitro, involves a switch in their metabolism and the utilization of the hexose-monophosphate shunt. This response of the epithelial rests is common to other epithelia when their supporting connective tissue is altered. It is suggested that the potential that activated cell rests have for dental cyst formation, as distinct from other epithelia, is due to their anatomic location. It is further suggested that intraepithelial cavitation of trabeculae of activated cell rests is the mechanism for initial cyst formation.

Sutural development: structure and its response to rapid expansion.

This fine structural study of the suture, its development, structure, and response to rapid expansion has shown that the sutural complex is best described in terms of the functional activity of two cell populations, namely, the osteocytic and fibrocytic series, which have the ability to remodel the tissues which they form. It is suggested that the previous detailed descriptions of differences in fiber orientation and vascular distribution reflect functional activity of a suture at any given time rather than immutable anatomic characteristics. Development of the suture and its rapid expansion showed many similarities in that growth during development and orthopedic expansion both separate the joint. If the initial inflammatory aspect of rapid expansion is ignored, the response of the suture is one of osteogenesis and fibrillogenesis, followed finally by remodeling. It is also suggested that sutural expansion involves injury followed by a proliferative repair phenomenon which, in other tissues, usually leads to the formation of scar tissue. However, the ability of sutural connective tissue fibroblasts to remodel ultimately leads to regeneration of the suture. Finally, programmed cell death has been shown to be an important feature in the development of the suture.

An Ultrastructural Study of Tooth Resorption in the Kitten

Eleven kittens of various ages were used to obtain teeth in situ at differing stages of exfoliation. The teeth were processed by routine techniques for examination by light and transmission electron microscopy. The dental hard tissues were eroded by odontoclasts supported by numerous blood vessels, fibroblasts, and macrophages. No evidence of intracellular collagen was found within any of these cells, indicating that helper cells are not required to remove the collagenous component of dentin and cementum. The loss of periodontal ligament during shedding involved the removal of cells and extracellular material. Two forms of fibroblastic cell death were identified: One, apoptotic cell death, involved condensation, and its occurrence suggests that exfoliation of deciduous teeth is a programed physiological event; the other occurred in cells containing many profiles of collagen and involved the selective disruption of the mitochondria and eventual dissolution of cytosol. This form of cell death has not been previously described and is significantly different from necrotic cell death, which was not observed during exfoliation. Some fibroblasts maintained a normal morphology. These various cellular responses suggest that phenotypically different populations of fibroblasts may exist in the periodontal ligament. Collagen removal was an extracellular occurrence which did not seem to involve increased phagocytotic activity by fibroblasts.

The extent and distribution of intratubular collagen fibrils in human dentine

Dentine of 27 permanent human teeth was examined by scanning electron microscopy. The teeth were incisors, canines, premolars and molars, ranging in age from 18 to 54 yr. Intratubular collagen was found in 65% of the dental tubules in inner dentine (closest to the pulp) with 16% of the tubules containing large collagen bundles occupying more than one-fifth of the lumen. In middle dentine the corresponding figures were 42 and 7%, and for outer dentine, 12 and 0% This pattern of distribution was the same for all tooth families examined and appeared to be unrelated to age.

An Immunocytochemical Study of the Human Odontoblast Process using Antibodies against Tubulin, Actin, and Vimentin

An immunofluorescence technique was applied at the light microscope level to human third molar coronal dentin in order to localize the intracellular components tubulin, vimentin, and actin. Third molars were split immediately upon extraction, and immersed in periodate-lysine-paraformaldehyde fixative. The crowns were demineralized, dehydrated, and wax-embedded, and 6-μm sections were prepared. The sections were post-fixed in -20°C acetone, and then incubated with monoclonal mouse anti-tubulin, anti-vimentin, or anti-actin antibodies, followed by fluorescein-conjugated sheep anti-mouse immunoglobulins. Intratubular immunofluorescence labeling for tubulin and vimentin was very similar in pattern and intensity and extended to the dentino-enamel junction. In contrast, the actin labeling appeared less intense and more punctate, and was located primarily in the pulpal half of the crown, although some labeling was detectable up to the dentino-enamel junction. The presence of tubulin-, vimentin-, and actin-containing structures extending to the dentino-enamel junction supports the hypothesis that the odontoblast process does extend to the dentino-enamel junction in the human, and is in agreement with earlier studies of rat molars.

Formation of supporting bone in association with periodontal ligament organization in the mouse.

Abstract Tritiated proline has been used as a marker for bone formation in association with tooth development in mice from birth to 24 days. The use of this marker has shown that bone deposition occurs on the socket wall in association with the organization of the periodontal ligament. The possible origin of the cells forming this bone is discussed and it is suggested that they originate from a layer of ectomesenchymal cells investing the tooth germ.

Development of a gomphosis by tooth germ implants in the parietal bone of the mouse

Abstract First molar tooth germs from 1-day-old mice were implanted into I mm holes prepared in the parietal bones of adult mice and left for 11, 14, 18 and 24 days. Seventy-four of 94 implanted tooth germs continued development with the formation of roots, periodontal ligament and new bone. This new bone fused with the old parietal bone thus establishing a true gomphosis between tooth and parietal bone.

Fine structural localization of alkaline phosphatase in relation to enamel formation in the mouse molar

Abstract Enzyme activity was localized to the stratum intermedium throughout amelogenesis but occurred in the ameloblasts only with the onset of enamel maturation. Its localization was to the striated border of the maturative ameloblast. It is suggested that the appearance of enzyme activity within the ameloblasts at this stage of enamel formation is related to calcium transport.

Reaction Paper: Session I. Odontoblasts

It is appropriate that this workshop begin with an extensive discussion of the odontoblast, without which there would be no dentin. This may seem a trite and obvious statement, but it is necessary, for as this workshop probes ever more deeply into the nuances of dentin and pulp structure, the central role of the cell can easily be forgotten. The first three papers presented can be summarized in three words: where, what, and how. Where do the odontoblasts come from; what are they like, and how do they function? I would like to react to all three papers within the framework of these questions.