The cytology of the dental follicle and adjacent alveolar bone during tooth eruption in the dog

Critical Reviews in Oral Biology & Medicine

Frazier‐Bowers

D’Souza

2002

334

239

Tooth eruption is a complex and tightly regulated process that involves cells of the tooth organ and the surrounding alveolus. Mononuclear cells (osteoclast precursors) must be recruited into the dental follicle prior to the onset of eruption. These cells, in turn, fuse to form osteoclasts that resorb alveolar bone, forming an eruption pathway for the tooth to exit its bony crypt. Some of the molecules possibly involved in the signaling cascades of eruption have been proposed in studies from null mice, osteopetrotic rodents, injections of putative eruption molecules, and cultured dental follicle cells. In particular, recruitment of the mononuclear cells to the follicle may require colony-stimulating factor-one (CSF-1) and/or monocyte chemotactic protein-1 (MCP-1). Osteoclastogenesis is needed for the bone resorption and may involve inhibition of osteoprotegerin transcription and synthesis in the follicle, as well as enhancement of receptor activator of NF B ligand (RANKL), in the adjacent alveolar bone and/or in the follicle. Paracrine signaling by parathyroid-hormone-related protein and interleukin -1␣, produced in the stellate reticulum adjacent to the follicle, may also play a role in regulating eruption. Osteoblasts might also influence the process of eruption, the most important physiologic role likely being at the eruptive site, in the formation of osteoclasts through signaling via the RANKL/OPG pathway. Evidence thus far supports a role for an osteoblast-specific transcription factor, Cbfa1 (Runx2), in molecular events that regulate tooth eruption. Cbfa1 is also expressed at high levels by the dental follicle cells. This review concludes with a discussion of the several human conditions that result in a failure of or delay in tooth eruption.

Section: (C) Cellular Eventsmentioning

confidence: 99%

Cellular, Molecular, and Genetic Determinants of Tooth Eruption

Critical Reviews in Oral Biology & Medicine

Frazier‐Bowers

D’Souza

2002

334

239

“…To accomplish this requires the presence of the dental follicle, a loose connective tissue sac that surrounds the unerupted tooth. Specifically, mononuclear cells (osteoclast precursors) are recruited to the follicle [2,3] where they fuse to form osteoclasts for alveolar bone resorption of the eruption pathway. In the first mandibular molar of the rat, the maximal number of mononuclear cells and osteoclasts are seen at day 3 [3,4] and this correlates with the maximal gene expression of 2 chemotactic molecules in the follicle -colony stimulating factor-1 (CSF-1) [5] and monocyte chemotactic protein-1 (MCP-1) [6].…”

Section: Introductionmentioning

confidence: 99%

A DNA microarray analysis of chemokine and receptor genes in the rat dental follicle—Role of secreted frizzled-related protein-1 in osteoclastogenesis

Liu

2007

Bone

Self Cite

The dental follicle, a loose connective tissue sac that surrounds the unerupted tooth, appears to regulate the osteoclastogenesis needed for eruption; i.e., bone resorption to form an eruption pathway. Thus, DNA microarray studies were conducted to determine which chemokines and their receptors were expressed chronologically in the dental follicle, chemokines that might attract osteoclast precursors. In the rat first mandibular molar, a major burst of osteoclastogenesis occurs at day 3 with a minor burst at day 10. The results of the microarray confirmed our previous studies showing the gene expression of molecules such as CSF-1 and MCP-1 in the dental follicle cells. Other new genes also were detected, including secreted frizzled-related protein-1 (SFRP-1), which was found to be down-regulated at days 3 and 9. Using rat bone marrow cultures to conduct in vitro osteoclastogenic assays, it was demonstrated that SFRP-1 inhibited osteoclast formation in a concentration-dependent fashion. However, with increasing concentrations of SFRP-1, the number of TRAP-positive mononuclear cells increased suggesting that SFRP-1 inhibits osteoclast formation by inhibiting the fusion of mononuclear cells (osteoclast precursors). Co-culturing bone marrow mononuclear cells and dental follicle cells demonstrated that the dental follicle cells were secreting a product(s) that inhibited osteoclastogenesis, as measured by counting of TRAP-positive osteoclasts. Adding an antibody either to SFRP-1 or OPG partially restored osteoclastogenesis. Adding both anti-SFRP-1 and anti-OPG fully negated the inhibitory effect of the follicle cells upon osteoclastogenesis. These results strongly suggest that SFRP-1 and OPG, both secreted by the dental follicle cells, use different pathways to exert their inhibitory effect on osteoclastogenesis. Based on these in vitro studies of osteoclastogenesis, it is likely that the down-regulation of SFRP-1 gene expression in the dental follicle at days 3 and 9 is a contributory factor in allowing the major and minor bursts of osteoclastogenesis to occur. Thus, inhibition of SFRP-1 gene expression in combination with inhibition of OPG gene expression likely are critical events in enabling alveolar bone resorption to occur such that teeth will erupt.

“…The major cellular event that occurs in the follicle just prior to or at the onset of prefunctional eruption (movement of tooth within the bony crypt) is an influx of mononuclear cells (monocytes) into the follicle (Marks et al, 1983;Wise et al, 1985Wise et al, , 1989. Concurrent with this is an increase in the number of osteoclasts in the bony crypt, osteoclasts that are required for the resorption of alveolar bone.…”

Section: Discussionmentioning

confidence: 99%

Localization of epidermal growth factor and its receptor in mandibular molars of the rat prior to and during prefunctional tooth eruption

Lin

Fan

1992

Developmental Dynamics

Self Cite

Immunoperoxidase localization of epidermal growth factor receptors (EGFR) and epidermal growth factor (EGF) itself was examined in rat first and second mandibular molars postnatally from day 0 to 12. The results showed that the dental follicle stained heavily for EGFR from day 0 to 8, declined in staining at day 9, and was devoid of stain from day 10 onward. Preosteoblasts and osteoblasts of alveolar bone also stained and lesser staining of ameloblasts and odontoblasts was observed. Except for staining of occasional isolated cells, the stellate reticulum did not stain. Light staining of the dental pulp of the first mandibular molar was seen from day 0 onward but the pulp of the second molar did not stain until approximately day 6. With respect to EGF, the dental follicle also stained for it until day 12. The ameloblasts stained more intensely for EGF than for EGFR. Because injections of EGF cause premature eruption of teeth and because the presence of a dental follicle is necessary for eruption, this study suggests that EGF could have its effect on the follicle as seen by the presence of EGFR receptors on the follicle. Moreover, because EGF exerts its effects early (day 0-3) to cause eruption and because the influx of monocytes into the follicle to form osteoclasts for bone resorption for eruption occurs early, the heavy staining for EGFR in the follicle early followed by the absence of staining at day 10 correlates chronologically with the key molecular and cellular events of eruption. Finally, the presence of EGF in the follicle, as well as enamel organ, could provide an endogenous source of EGF to regulate tooth eruption, either by an autocrine or a paracrine effect. Thus, the localization of EGFR and EGF in the dental follicle coupled with the chronology of localization suggests that EGF could play a physiological role in tooth eruption. o 1992 Wiley-Liss, Inc.