Dental follicle

The dental follicle, also known as dental sac, is made up of mesenchymal cells and fibres surrounding the enamel organ and dental papilla of a developing teeth. It is a vascular fibrous sac containing the developing tooth and its odontogenic organ. The dental follicle (DF) differentiates into the periodontal ligament. In addition, it may be the precursor of other cells of the periodontium, including osteoblasts, cementoblasts and fibroblasts. They develop into the alveolar bone, the cementum with Sharpey's fibers and the periodontal ligament fibers respectively. Similar to dental papilla, the dental follicle provides nutrition to the enamel organ and dental papilla and also have an extremely rich blood supply. The dental follicle, also known as dental sac, is made up of mesenchymal cells and fibres surrounding the enamel organ and dental papilla of a developing teeth. It is a vascular fibrous sac containing the developing tooth and its odontogenic organ. The dental follicle (DF) differentiates into the periodontal ligament. In addition, it may be the precursor of other cells of the periodontium, including osteoblasts, cementoblasts and fibroblasts. They develop into the alveolar bone, the cementum with Sharpey's fibers and the periodontal ligament fibers respectively. Similar to dental papilla, the dental follicle provides nutrition to the enamel organ and dental papilla and also have an extremely rich blood supply. The formative role of the dental follicle starts when the crown of the tooth is fully developed and just before tooth eruption into the oral cavity. Although tooth eruption mechanisms have yet to be understood entirely, generally it can be agreed that many factors, together, affect the tooth eruption process which is why it is very difficult to differentiate the causes and effects. There have been many theories proposed for tooth eruption. Ideas such as remodelling of the alveolar bone, root elongation and to a certain extent, the most probable reasoning for tooth eruption in human beings is the formation of the periodontal ligament. Bone remodelling of the jaws has been associated to tooth eruption such that in the pre-eruptive phase of a tooth, the natural pattern of growth of the maxilla or mandible would theoretically move teeth by the selective deposition and reabsorption of bone in the adjacent surroundings of the tooth. A sequence of experiments in dogs does provide the most reliable substantiation to prove that bone remodelling is a cause of tooth movement. When an eruption is stopped by wiring the tooth germ on to the lower margin of the mandible or when the dental follicle remains undisturbed as the developing pre-molar is removed, osteoclasts enlarge the gubernacular canal while an eruptive pathway develops within the bone covering over the enucleated tooth. However, no eruptive pathway will develop if the dental follicle is removed. Furthermore, the replica will erupt with the development of an eruptive pathway as long as the dental follicle is preserved when an exact silicone or metal duplicate replaces the tooth germ. Such observations should be examined judiciously and in great detail. Firstly, eruptive pathways have unmistakably been demonstrated to develop in bone deprived of a budding or growing tooth. Secondly, they provided evidence to prove that the dental follicle is involved in the process. Therefore, it is only when concurrent bone deposition can be confirmed at the base of the crypt and inhibition of such bone deposition can be demonstrated to show interference with tooth eruption, then the conclusion that an eruptive pathway forming within bone means that bony remodelling is the cause for tooth formation. In many studies, with the usage of tetracyclines as indicators of bone deposition have proven that bone resorption is principal activity in the fundus of an alveolus in a number of species, including human beings. For example, in human beings, the base of the crypt of the permanent first molars and permanent third molars will repeatedly reabsorb as the eruption of these teeth occur, although, in the second molars and second premolars, there will be some bone deposition on the crypt floor. For the circumstance of a dormant duplicate’s demonstrated eruption, many would think that the bony remodelling would be the only reason. However, as per what will be discussed next, it can be concluded that follicular tissue is accountable for this movement as supported by pieces of evidence. Furthermore, in some recent research, it has been observed that alveolar bone growth at the base of the crypt is a prerequisite for molar tooth eruption in rats. Undoubtedly, more attention needs to be given to the intraosseous tooth eruption. Regardless of whether bone growth is a main moving force, it can widely be agreed that for tooth eruption to happen, the dental follicle is required and that, as will be discussed later, the dental follicle regulates bone remodelling. Researches show a repeated series of cellular activities which involves the reduced dental epithelium and the follicle linked to tooth eruption that assists bone absorption and connective tissue degradation. With the lack of colony-stimulating factor 1, a factor that encourages differentiation of osteoclasts, in osteopetrotic animals, no mechanism for bone removal is present and therefore eruption is prevented. The eruption will happen when differentiation of osteoclasts is allowed due to local administration of the colony-stimulating factor 1. Proteases, which is produced by the reduced enamel epithelium, results in a path of least resistance as it promotes the breakdown of connective tissue. When stimulating alveolar bone growth at the base of the crypt, expression of the bone morphogenetic protein-6 in the dental follicle may also be necessary. It is also thought that signalling between the dental follicle and the reduced enamel epithelium exists. This signalling could be a plausible reason for the noteworthy regularity of eruption timings because the enamel epithelium is most possibly programmed as part of its functional life cycle. Signalling would also aid in explaining why radicular follicle, that is not related to reduced enamel epithelium, is involved in the formation of the periodontal ligament but does not experience degeneration.