Answer by Anirudha Agnihotry:
I did a literature review for a project, and this was a part of it. I have selected the related part from that review and presented at the end. For detailed answers please scroll down and read.
In short, the root of the adult teeth grow and the bone surrounding them remodel, which gets the adult tooth moving in upward direction, and baby teeth are eventually shed. It is also supported by hormones and so protein dissolving enzymes in a complex fashion.
There is a video about the process, followed by a detailed overview
CAUSES OF TOOTH ERUPTION
Some researchers have proposed that the forces for tooth eruption come from the elongation of the root while growing. To negate this belief, there is evidence of eruption of rootless teeth. Thus, it cannot be considered as a theory that explains the mechanism. It may, however, accelerate the process.(1)
Alveolar Bone Remodeling
Alveolar bone growth below the developing root of the tooth is also one school of thought that was adapted in the eruption model. In cases of osteopetrosis and cleido-cranial dysplasia, eruption of teeth doesn’t occur because alveolar bone growth involving turnover (resorption and formation) is required during tooth eruption. Bone removal and bone apposition is polarized around erupting tooth and these events depend upon the adjacent parts of the dental follicle. (1,2)
The idea of periodontal ligament creating the eruptive force was oversold by the studies done on rodents, which show continuous eruption, i.e., the eruption continues indefinitely. For the human model of limited eruption, periodontal forces are not considered to be the main cause as there is evidence of eruption of rootless teeth, which do not have periodontium.(2,3)
Regional changes in vascular pressure have long been proposed as a force behind eruption, but the evidence for this phenomenon is on both sides, i.e., in support as well as in opposition. It was showed in a study that injection of a vasodilator above the root apex caused a transient increase in the rate of eruption, whereas injection of a vasoconstrictor caused a decrease or intrusion. In another study, decreased eruption rate was found with systemic infusion of angiotensin II, as it increased mean arterial pressure. There has been some contradictory evidence as well to this belief.(4)
Risinger and Proffit experimented on premolar eruption in human subjects and established a relation that a circadian rhythm of eruption existed. They concluded the effects to be because of the Human Growth Hormone and the nature of eruption was cyclic, peaking in the evening and intrusion occurred with eating of the meals. Later delayed eruption was reported in patients with deficient thyroid hormones, supporting the former.(5) In another study, it was shown that the inhibition of crown eruption accelerates the elongation of root at apex; and mesial bone resorption with cell proliferation with increased enamel thickness in apically.(6) This might be the pattern of eruption with daily hormonal changes. It has also been shown that stress induced in pregnant mice lead to delayed eruption in the offspring, showing that certain hormones released in stress may have deleterious effect on the process of tooth eruption in the pups.(7)
Role of proteases in tooth eruption
Through a series of experiments on protease activity and dental follicles, Gorski and Marks(8) postulated the potential roles of proteases in the tooth eruption, which are as follows:
1. Degradation of capillary basement membrane sites, thus facilitating entry of osteoclast precursor cells into folicle from blood.
2. Degradation of cell-matrix contact regions leading to reorganization of cell-cell and cell-matrix interactions necessary for periodontal ligament development.
3. Break down of matrix-bridging molecules leading to reorganization of matrix and establishment of new cell-cell and cell-matrix contacts and matrix-binding sites.
4. Release of active growth factors from plasma membrane bound precursors and matrix binding sites.
Molecular regulation of osteoclastogenesis and osteogenesis.
Based on numerous studies that include gene deletions, timing of gene up-/down-regulation, immunocytochemistry, osteopetrotic rodents, and in vitro assays, a subjective scale is presented of the importance of various mediators in intra-osseous tooth eruption and orthodontic tooth movement. Scale values are as follows: (-) not required or insufficient data; (+) slight effect; (++) moderate effect; (+++) greatest effect. (Wise and King 2008)
Osteoclastogenesis. Colony stimulating factor-1 (CSF-1) and monocyte chemotactic protein-1 (MCP-1) are chemokines for monocytes and are secreted by the dental follicle cells. CSF-1 increases the activity of receptor activator of nuclear factor-kappa B ligand (RANKL). The decrease in osteoprotegerin expression effected by CSF-1 and increasing the RANKL creates a major burst of osteoclastogenesis to occur. Another protein from the stellate reticulum is parathyroid-hormone-related protein (PTHrP), which, if not expressed, leads to non-eruption of tooth. PTHrP enhances vascular endothelial growth factor (VEGF) gene expression at a later stage in the dental follicle cells. VEGF increases RANKL activity and osteoclasts are differentiated and another burst of osteoclastogenesis is observed. The level of yet another inhibitor, SFRP1, is also down regulated during eruption, but it is not yet known what molecule inhibits SFRP1 in the upper half of dental follicle.(9,10)
These observations are shown in the figure that follows, which is a depiction of a study done in the mice. At day 3, CSF-1 is highest and by day 10, VEGF is high and plays the major role in osteoclastogenesis.11
(Wise and King 2008)
Osteogenesis. Bone morphogenic protein-2 (BMP-2) is found to be expressed in the basal half of dental follicle more than its coronal counterpart. BMP-2 is responsible for osteogenesis. A strong correlation exists between BMP-2 expression in the basal one-half of the dental follicle and the presence of trabecular bone (osteogenesis) in the basal portion of the socket. The expression of an important transcription factor for osteoblast differentiation, core-binding factor a1 (Cbfa1) or Runx2, is seen as well in the dental follicles of mice. Also, membrane-type 1 matrix metalloproteinase (MT1-MMP) -deficient mice show a large accumulation of phagosomes containing collagen fibrils, and so it is also believed to aid in the eruption process.11 MT1-MMP in the periodontal ligament (which is derived from dental follicle), is responsible for appropriate remodeling of connective tissue and the bone interface, which is likely is needed for alveolar bone formation to occur. This, in turn, might propel the tooth upwards.(10)
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3. Fleischmannova J, Matalova E, Sharpe PT et-al. Formation of the tooth-bone interface. J. Dent. Res. 2010;89 (2): 108-15.
4. Marks SC, Schroeder HE. Tooth eruption: theories and facts. Anat. Rec. 1996;245 (2): 374-93.
5. Lee CF, Proffit WR. The daily rhythm of tooth eruption. Am J Orthod Dentofacial Orthop. 1995;107 (1): 38-47.
6. Miwa T, Matsuzaka K, Inoue T. Effect of interrupted eruption on the enamel organ of the rat incisor. Zoology (Jena). 2013;116 (2): 90-8.
7. Fontanetti PA, De lucca RC, Mandalunis PM et-al. Impairment of rat tooth eruption in pups born to mothers exposed to chronic stress during pregnancy. Arch. Oral Biol. 2013;58 (11): 1643-51.
8. Gorski JP, Marks SC. Current concepts of the biology of tooth eruption. Crit. Rev. Oral Biol. Med. 1992;3 (3): 185-206.
9. Wise GE, King GJ. Mechanisms of tooth eruption and orthodontic tooth movement. J. Dent. Res. 2008;87 (5): 414-34.
10. Wise GE. Cellular and molecular basis of tooth eruption. Orthod Craniofac Res. 2009;12 (2): 67–73 .