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I.

INTRODUCTION Tooth eruption is an essential process for the survival of many species

and although the movement of teeth into function has been the subject of extensive research, there is no consensus as to the mechanisms involved. The term tooth “tooth eruption� generally refers to the appearance of some part of the tooth above the surface of the gingiva. However, eruption actually includes the entire embryological process from the formation of the tooth germs, in the mandible and maxilla, to calcification, crown formation and root formation. The root is only about 1/3 rd formed when the crown begins to erupt into the oral cavity. Not only is this embryological process a part of the eruption, so is the long process of occlusal development. Thus, the emergence of teeth into the oral cavity is only a part of the total eruption process.

I.

TOOTH MOVEMENTS The teeth develop within the tissues of the jaw. Thus for the teeth to

become functional, considerable movement is required to bring them into the occlusal plane. The movements teeth make, are complex and may be described in general terms under the following headings: 1. Pre-eruptive tooth movement - which is made by both the deciduous and permanent tooth germs within the tissues of the jaw before they begin to erupt. 2. Eruptive tooth movement - made by a tooth to move from its position within the bone of the jaw to its functional position in occlusion.

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3. Post-eruptive tooth movement - those which maintains the position of the erupted tooth in occlusion while the jaws continue to grow and to compensate for occlusal and proximal wear of the tooth. Although this categorization of tooth movement is convenient for descriptive purposes, it must be recognized that, what is being described is a complex series of events occurring in a continuous process. As a result, other categorizations exist. For instance, some describe tooth movement as having pre-functional and functional phases. 1.

Pre-Eruptive Tooth Movements When the deciduous tooth germs first differentiate, they are extremely

small and there is a good deal of space for them in the developing jaw. Because the tooth germs grow rapidly, however they become crowded together, particularly in the anterior region of the jaw. This crowding is gradually alleviated by the lengthening of the jaws, which permits the second deciduous molar tooth to move backward and the anterior tooth germs to move forward. At the same time, the tooth germs are also moving bodily outward and upward or downward as the case may be, as the jaws increase in length as well as in width and height. The permanent tooth germs develop on the lingual aspect of their deciduous predecessors in the same bony crypt. From this position, the tooth germs shift considerably as the jaws develop. For example, the incisors and the canines eventually come to occupy a position, in their own bony crypts, on the lingual of the roots of their deciduous predecessors, while the premolar tooth germs, also in their own crypts, are finally positioned between the divergent roots of the deciduous molars.

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The permanent molar tooth germs which have no predecessors, develop from the backward extension of the dental lamina. At first there is little room in the jaws to accommodate those tooth germs, so that in the upper jaw the molar tooth germs first develop with their occlusal surfaces facing distally and can swing into position only when the maxilla has grown sufficiently to provide room for such movement. In the mandible, the permanent molars develop with their axis showing a mesial inclination which becomes vertical only when sufficient jaw growth has occurred. These pre-eruptive movements of both deciduous and permanent tooth germs are best thought of as the movements required to place the teeth within the jaw in a position for eruptive tooth movement. Analysis has shown that these pre-eruptive movements of the tooth are a combination of two factors. The first factor is the total bodily movement of the tooth germs and the second factor is growth, in which one part of the tooth germ remains fixed while the rest continues to grow, leading to a change in the centre of the tooth germ. This growth explains, for example, how the deciduous incisors maintain their position relative to the oral mucosa as the jaws increase in height. As pre-eruptive movement occur in an intraosseous location, such movement is reflected in the patterns of bony remodeling within the crypt wall. For example during bodily movements in a mesial direction, bone resorption occurs on the mesial surface of the crypt wall and bone deposition occurs on the distal wall as a filling in process. During eccentric growth, only bony resorption occurs, thus altering the shape of the crypt to accommodate the altering shape of the tooth germ.

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2.

Eruptive Tooth Movement During the eruptive phase of physiologic tooth movement, significant

developmental changes occur, including the formation of roots, periodontal ligament and dentogingival junction of the tooth. Root formation is initiated by the proliferation of Hertwig’s epithelial root sheath. The forming root first grows toward the floor of the bony crypt and as a result, there is resorption of bone in this location to provide room for the advancing root tip. However, with the onset of eruptive tooth movement, (probably coincident with the periodontal ligament formation) space is created for the forming root and resorption no longer occurs on the floor of the crypt. Indeed, in some instances the distance moved by the tooth outstrips the rate of root formation and bone deposition occurs on the crypt floor. As the roots of the tooth form, important changes associated with the development of the supporting apparatus of the tooth occur in the dental follicle. -

There is bone deposition on the crypt wall.

-

Cement deposition on the newly formed root surface.

-

Organization of a periodontal ligament from the dental follicle.

These changes lag behind root formation. There are a number of important histologic features in the periodontal ligament that are important in explaining eruptive tooth movement. First, is the occurrence of cell to cell contacts of the adherens type between periodontal ligament fibroblasts. Second, is the demonstrated presence of contractile elements in ligament fibroblasts. Third, is the occurrence of a structure called fibronexus. This describes a morphologic relationship between intracellular microfilaments in the fibroblast, 4


a corresponding increased density of fibroblast cell membrane, extracellular filaments and fibronectin. Fibronectin is a sticky glycoprotein which sticks to a number of extracellular components including collagen. Fourth, is the active ingestion and degradation of old collagen fibrils by many of the fibroblasts of the ligament and the convenient formation of new collagen fibrils. Thus the continual degradation and synthesis of collagen by fibroblasts permit the remodeling of the principal fibre bundles of the periodontal ligament.

Significant changes occur within the tissues that cover the erupting tooth. There is a loss of intervening connective tissue between the reduced enamel epithelium covering the crown of the tooth and the overlying oral epithelium. Because of this loss, the two epithelia proliferate and form a solid plug of cells in advance of the erupting tooth. The central cells of this epithelial mass degenerate and form an epithelium lined canal through which the tooth erupts without any haemorrhage. This epithelial cell mass is also involved in the formation of the dentogingival junction.

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Interestingly, once the tooth erupts into the oral cavity, it continues to erupt at the same rate of about 1mm every 3 months, only slowing as it meets its antagonist in the opposing arch. This suggests that the resistance to the force of tooth eruption provided by the overlying connective tissue is minimal. Root formation, however, is not yet complete, and because further occlusal movement is restricted, additional root growth is accommodated by removal of bone on the socket floor. The above description generally applies to all the teeth. Successional teeth, however possess an additional anatomic feature, the gubernacular canal and its contents, the gubernacular cord which may have an influence on eruptive tooth movement. When the successional tooth germ first develops within the same crypt as its deciduous predecessor, bone surrounds both tooth germs but does not complete close over them. As the deciduous tooth erupts, the permanent tooth germ becomes situated apically and entirely enclosed by bone, except for a small canal that is filled with connective tissue and often contains epithelial remnants of the dental lamina. This connective tissue mass is termed the ‘gubernacular cord’ and it may have a function in guiding the permanent tooth as it erupts. Once the erupting tooth appears in the oral cavity, it is subjected to environmental factors that help determine its final position in the dental arch. 6


Muscle forces from the tongue, the cheeks, and the lips play on the tooth, as do the forces of contact of the erupting tooth with other erupted teeth. A sustained muscular force of only 4 to 5 grams is sufficient to move a tooth. The childhood habit of thumb sucking is an obvious example of environmental determination of tooth position. 3. Post Eruptive Movement Post eruptive movements are those made by the tooth after it has reached its functional position in the occlusal plane. They may be divided into three categories: 1. movements made to accommodate the growing jaws. 2. those made to compensate for continued occlusal wear. 3. those made to accommodate interproximal wear. a.

Accommodation for growth They are seen histologically as a readjustment of the position of the

tooth socket, achieved by the formation of new bone at the alveolar crest and on the socket floor to keep pace with the increasing height of the jaws. Recent studies have shown that this readjustment occurs between the ages of 14 to 18, when active movement of the tooth takes place. The apices of the teeth move 2 to 3 mm away from the inferior dental canal (regarded as a relatively fixed reference point). This movement occurs earlier in girls than in boys and is related to the burst of condylar growth that separates the jaws and teeth, permitting further eruptive movement. Although this movement is seen as remodeling of the socket, it must not be assumed that this bony remodeling brings about tooth movement.

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b.

Compensation for occlusal wear The axial movement a tooth makes to compensate for occlusal wear is

most likely achieved by the same mechanism as eruptive tooth movement. It is often stated that the compensation for occlusal wear is achieved by continued cementum deposition around the apex of the tooth, but the deposition of cementum in this location occurs only after the tooth has moved. c. Accommodation for interproximal wear Wear also occurs at the contact points between teeth on their proximal surfaces the extent of this wear can be considerable (more than 7 mm in the mandible). This interproximal wear is compensated for, by a process known as mesial or approximal drift. There are two, possibly three factors that bring about mesial drift. They are: i. occlusal force ii. ligament contraction and possibly iii. soft tissue pressures. i.

Anterior component of occlusal force When the teeth are brought into contact, for example, when the jaws are

clenched, a forwardly directed force is generated. That this is so can be easily demonstrated by placing a steel strip between the teeth and showing that more force is required to remove it when the jaws are clenched. The anterior force is the result of the mesial inclination of most teeth and the summation of the intercuspal planes producing a forwardly directed force. In the case of incisors which are inclined labially, it would be expected that any anterior component of force would move them in the same direction. Incisors in fact moves mesially but this can be explained by the billiard ball analogy.

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That cuspal inclination is a significant factor can be demonstrated by selectively grinding cusps in such a way so as to either enhance or reverse the direction of the occlusal force. When opposing teeth were removed thereby eliminating the biting force, the mesial migration of teeth were slowed but not halted indicating the presence of some other force, and here the transseptal fibres of the periodontal ligament have been implicated. ii.

Contraction of transseptal fibres The periodontal ligament has an important role in maintaining tooth

position, and it is suggested that its transseptal fibres running between adjacent teeth across the alveolar process draw neighbouring teeth together and maintain them in contact. There is some evidence to support this. For example, it is known that relapse of orthodontically moved teeth is much reduced if gingivectomy is done, that is the transseptal ligament is removed. It has been demonstrated experimentally that in bisected teeth, the two halves separate from each other. If however, the transseptal ligaments are previously cut, this separation does not occur. By disking away proximal contacts, room is provided for the tooth to move to reestablish contact. 9


iii.

Soft tissue pressures It does not have a major role in tooth movement. The pressures

generated influence tooth position, even if it does not cause tooth movement.

III. THEORIES OF TOOTH ERUPTION The mechanism that brings about tooth movement is debatable. There are numerous theories of tooth eruption which is usually a reflection of incomplete understanding. All these theories have contributed to and provoked research into various aspects, to support or refute hypotheses which are now briefly reviewed. 1.

Pulp Theory This theory suggests that a propulsive force is generated by extrusion of

the pulp through three mechanisms; first growth of dentin, secondly, interstitial pulp growth and thirdly, hydraulic effects within the vasculature. Perhaps the most damning evidence against this theory is the work of Herzberg and Schour (1941) who removed the pulp of rodent incisors and found that its eruption rates were unaffected. 2.

Vascular Theory The mechanisms behind this theory to some extent overlaps the pulp

theory. The force of eruption comes from the pressure in the blood vessels within or below the tooth. This theory has been discounted by some for the same reasons as the pulp theory. In addition, use of hypotensive drugs appears to have no effect on the eruption rates. However, a critical review by Moxham suggests that at least part of the eruptive force is generated by a non-functional force.

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3.

Root elongation theory This theory attributes tooth eruption to elongation of the roots. It

suggests that the tooth erupts as a result of root pushing against an immovable base. Root formation appears to be the obvious cause of tooth eruption, since it undoubtedly causes an overall increase in the length of the tooth which must be accommodated either by the root growing into bone of the jaw, by increase in height of the jaw, or by crown of the tooth moving occlusally. It is the latter movement, of course that occurs but it does not follow that root growth is responsible. If a continuously erupting tooth, such as a rodent incisor or a guinea pig molar is prevented from erupting by pinning the tooth to the bone, root growth continues and is accommondated by resorption of some bone at the base of the socket and a buckling of the newly formed root. Such a simple experiment yields two conclusions: first, that root growth produces a force; second, that this force is sufficient to produce bone resorption. At one time, it was proposed that a structure called “Cushion hammock� ligament was strung across the base of the socket and when the growing root impinged on it. This structure acted as a sling, translating downward root growth into eruptive tooth movement. Careful histologic study has found no such ligament. It must therefore be concluded that some force other than root growth is moving the tooth to provide room for the newly formed root tissue. Furthermore, Marks and Cahill (Arch. Oral Biol.; 1984) using young dogs, took teeth at the beginning of eruption, removed their pulps and killed the periodontal ligament cells by freeze thawing. These inert rootless teeth with no periodontal ligaments were reimplanted and still managed to erupt by compensatory bone growth. Thus, although root growth can produce a force, it cannot be translated into eruptive tooth movement unless there is some structure at the base of the tooth capable of withstanding the force. 11


4.

Alveolar bone growth The importance of bone growth in tooth eruption was demonstrated with

a series of classical experiments by Brash (1928) using madder fed pigs. Madder is a dye which binds to newly formed bone and Brash noticed large amounts of bone laid down between the crypts of erupting teeth. These observations have been confirmed (Marks and Cahill 1980), but although bone formation is clearly involved in tooth eruption, cause and effect are still at the phenomenology stage. 5.

Periodontal ligament theory This theory suggests that the impetus for tooth eruption is derived from

the periodontal ligament. Evidence for this came from some brief observations by Moxham and Berkovitz (Arch. Oral Biol.; 1974) where root transsection failed to prevent the incisor segment superfacial to the transsection from erupting. This strongly implicates the periodontal ligament in the eruption process, and suggests that there is little contribution from alveolar bone, root growth and indeed pulp pressure. Evidence against this theory includes studies with lachyritic compounds, such as β-aminoproprionitrile. They inhibit intermolecular crosslinking of the polypeptide chains in the collagen molecule and should therefore inhibit the teeth from erupting. Despite adminstration of these drugs, rat incisors continue to erupt normally. It has already been indicated that fibroblasts have the ability to contract, but for such contractions to bring about tooth movement, a number of other conditions must be met. There must be some mechanism to summate the contractile forces of a number of fibroblasts; the fibroblasts must have something to pull on (collagen fibre bundles?) which must also be firmly attached to the tooth and be correctly oriented. The numerous cell to cell

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contact between fibroblasts could be involved in summating contractile force. The fibronexus and associated fibronectin could transmit this force to the collagen fibre bundles. These bundles in turn are firmly attached to the bone and the tooth in the correct position to bring about tooth movement. Finally, they have the ability to remodel after the tooth moves. In summary, then the force moving the tooth is most likely generated by the contractile property of the ligament fibroblast, but a number of other conditions must exist to translate this contraction into tooth movement. Eruption must therefore be considered a multifactorial phenomenon. The periodontal ligament theory has also gained some support from tissue culture experiments. If a fibroblast is cultured on a substrate on which it can move, it vibrates using contractile mechanisms generated by its cytoskeleton. The actin molecule has a particularly prominent role. As the fibroblast moves, it elongates on the leading edge and leaves the trailing end of the cell adherent to the substrate. Eventually the latter edge will detach. If these cells are cultured on thin silicon sheets, then as they move, the contractile element is sufficiently strong to cause the rubber to wrinkle. This effect can also be demonstrated when these cells are embedded in three dimensional gels and this is true for fibroblasts derived from the periodontal ligament. This model has been adapted to show that periodontal ligament fibroblasts are capable of generating sufficient contractile force to lift a piece of root, against gravity, towards the top of a tissue culture well (Arch. Oral Biol.; 1983). Direct evidence of this tractional effect is not available but these models prove that periodontal ligament has some role in the process of eruption.

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6.

Genetic input If tooth eruption is to be explained at the cellular and molecular level, a

degree of genetic control is highly likely in normal development of occlusion. Incisors erupt before premolars and this process of eruption is often disturbed in a number of genetic disorders. A classification of this has been presented by Caulk (1988). These comprise: a.

inhibited defects, primarily involving enamel - amelogenesis imperfecta.

b.

syndromes with enamel involvement.

c.

disorders associated with supernumerary teeth and / or crowding of teeth.

d.

growth retardation syndromes.

e.

conditions associated with tissue overgrowth of the gingiva and hyperplastic frenula.

f.

miscellaneous disorders (these include premature exfoliation such as Hypophosphatasia, Juvenile Periodontosis and Papillon Lefevre Syndrome). There is no simple explanation of tooth eruption and this biological

phenomenon is a multifactorial event. Biological sciences are more likely to offer clear, rational approaches to improve our understanding of tooth eruption. 7.

Hydrostatic pressure. This theory requires a higher pressure system, either within or around

the base of the tooth. It is known that teeth move in their sockets in synchrony with the arterial pulse, so local volume changes can produce limited tooth

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movement. Ground substance can swell from 30%-50% by retaining additional water, so this too could create pressure. But, since surgical excision of the growing root and associated tissue eliminate the periapical vasculature without stopping eruption, this means that the local vessels are not absolutely necessary for tooth eruption. 8. Follicular Theory This theory attributes a critical role to the dental follicle for the eruption of teeth. It seems unlikely that the dental follicle provides the eruptive force since fibre transsection fails to prevent eruptive movement. It seems more probable that the loose connective tissue of the dental follicle is a rich source of factors which are responsible for bone formation and resorption. Indeed, the follicle is capable of releasing cytokines, ericunosoids and growth factors but as our understanding of these factors increases, we’re likely to explain tooth eruption in terms of cellular and molecular interactions. Follicular Theory – Molecular Biology of Initiation of Tooth Eruption Further studies have been done regarding Follicular Theory through recent advances in Molecular Biology. Thanks to the pioneering experiments of Marks and Cahill, it was established that, in teeth of limited eruption, a tissue required for eruption is the dental follicle, a loose connective tissue sac that surrounds the tooth prior to eruption. Their studies showed that surgical removal of the follicle prevents eruption whereas leaving the follicle intact but substituting an inert object for the tooth results in eruption of the inert object (Marks & Cahill; 1984). At the cellular level there is an influx of mononuclear cells (monocytes) in the dental follicle which is the onset of active eruption (Marks et al.; 1983

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Wise et al.; 1985). Concurrent with the monocyte influx is an increase in the number of osteoclasts on the coronal positions of the bony crypt followed by a decrease that parallels monocyte decrease. Studies by Wise and Lan (1989) suggests that the influx of the monocytes contributes to the formation of osteoclasts to resorb alveolar bone for the tooth to escape its bony crypt. What is / are the molecular signal(s) that ultimately initiate the onset of tooth eruption as seen by the above cellular changes?. At least 4 molecules emerge as potential candidates because of their ability to accelerate eruption, their immuno localization, their gene expression or a combination of these. Perhaps the molecule that plays the most direct role in initating the cellular events of eruption is colony stimulating factor one (CSF-1). When these were injected into osteopetrotic (toothless) rats, the incisors erupted (Ilizuka et al.; 1992) and injection of CSF-1 in normal rats lead to eruption of first molars with increase in numbers of monocytes and osteoclasts (Cielinski et al.; 1995). A cascade of molecular signals is probably involved in stimulating the expression of CSF-1 for the onset of eruption. In particular, interleukin-1α (1L-1α) enhances the transcription of CSF-1 gene in rat dental follicle cells (Wise and Lin; 1994). Immunolocalization studies have shown that 1L-1α is present in the stellate reticulum (Wise et al.; 1995), the portion of enamel organ that is immediately adjacent to the dental follicle. Thus the 1L-1α might diffuse into the dental follicle to stimulate the dental follicle cells to express the CSF-1 gene. The expression of the 1L-1α gene may be regulated by epidermal growth factor (EGF). EGF, long known for its ability to stimulate precocious

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eruption of incisors in rodents (Cohen; 1962), also increases the amount of 1L-1α in the stellate reticulum following injection into rats (Wise et al.; 1995). Another molecule that might be involved in a cascade of signals leading to tooth eruption is transforming growth factor β1 (TGF- β1). Like 1L-1α TGF β1 immunolocalizes to the stellate reticulum and in vitro, its mRNA expression is enhanced

by

incubation

with

EGF.

Because TGF- β1 is a chemoattractant for monocytes, it is possible that TGF β1 could enter the capillaries adjacent to the dental follicle and attract monocytes to the follicle. Based on these above studies, a hypothesis of the molecular events of tooth eruption can be presented: 1. If EGF were the first signal there are at least three ways it could initiate eruption. 2. If EGF were not required, however, eruption could begin with a signal from TGF- β1. 3. Should EGF and TGF-β1 both not be required, eruption could begin with 1L-1α enhancing CSF-1 mRNA expression.

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IV. PATTERN OF ERUPTION OF TEETH The teeth of the deciduous dentition begin to appear in the mouth at about 6 months of age and the dentition is complete by 3 years. A majority of the permanent teeth appear in the mouth between 6 and 12 years of age, during this time teeth from both dentitions are present in the mouth, a phase known as mixed dentition. The teeth of both dentitions develop initially within the bones of the jaws and have to move bodily through the jaws to reach the oral cavity by the process of eruption. In addition, the deciduous teeth have to be shed or exfoliated to make room for their permanent successors. In the deciduous dentition, calcification of the crowns commences about a month after the completion of cytodifferentiation of the tooth germ. Calcification of all deciduous teeth begins before birth. Crown formation takes about 6 months to complete and the tooth appears in the mouth some 6 months after crown formation is achieved. When the teeth first appear, their roots are incomplete and are not fully formed until 18 months later. In the permanent dentition, the tooth germs are fully formed before birth for all but the second and third molars. Crown formation begins at varying times thereafter. In general, for the teeth of the permanent dentition, crown formation takes 3 years and the teeth appear in the oral cavity about 3 years after the crown is complete. Root completion is achieved about 3 years after eruption.

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The sequence of eruption is an important aide memoire; the first permanent molars erupt first at 6 years of age. The other teeth appear at approximately yearly intervals corresponding to their sequence of eruption. If the sequence and dates of eruption are remembered, the timing of other events may be calculated by simple addition or subtraction. Birth to Two Years The permanent incisors and canines first develop lingual to the deciduous tooth germs at the level of their occlusal surfaces and in the same bony crypt. As their deciduous predecessors erupt, they move to a more apical position and occupy their own bony crypts. First teeth to erupt are the mandibular central incisors. The usual eruption sequence in the primary dentition is as follows. First the central incisors, followed in order by the lateral incisors, first molars, canines and second molars. Mandibular teeth usually precede the maxillary teeth. This sequence is not always followed. Time of eruption is usually stated as 6 months of age for the maxillary primary centrals, 7-8 months for the mandibular primary laterals and 8 or 9 months for the maxillary primary laterals. At about 1 year, the first primary molars erupt. At around 16 months, the primary cuspids appear. Two years is usually given as the age for the second primary molars to appear. Two Years to Six Years By two and a half years of age, the deciduous dentition is usually complete and in full function. By three years of age, the roots of all deciduous teeth are complete. First permanent molar crowns are fully developed and the roots are starting to form. The crypts of the developing permanent second

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molars are now definite and can be seen in the space formerly occupied by the developing first permanent molars. Between three and six years of age, the development of the permanent teeth continues, with the maxillary and mandibular incisor teeth more advanced. From five to six years, just before the shedding of the deciduous incisors, there are more teeth in the jaws than at any other time. Space is quite critical within both the alveolar process and the deciduous dental arches themselves. Developing permanent teeth are shifting close to the alveolar border, the apices of the deciduous incisors are being resorbed; the first permanent molars are about ready to erupt. Very little bone exists between the permanent teeth and their crypts and the “front line” of deciduous teeth. [A cross section of the maxilla and mandible illustrates this remarkable phenomenon]. The complex interplay of forces makes it imperative that the integrity of the dental arch be maintained at this time. Loss of arch length through caries may make the difference between normal occlusion and malocclusion. It does not take very much to upset the delicate timetable of tooth formation, eruption and resorption within a viable osseous medium. Six Years to Ten Years Between six and seven years of age, the first permanent molars erupt into the mouth. As the upper and lower first permanent molars erupt, a pad of tissue overlying them creates a premature contact. Proprioceptive response conditions the patient against biting on this natural “bite opener” and thus the deciduous teeth anterior to the first permanent molar area erupt, reducing the overbite. About this time, the deciduous central incisors are lost and their permanent successors start their eruptive path toward contact with the incisors

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of the opposing arch. Usually the mandibular central incisors erupt first, followed by the maxillary permanent central incisors. These teeth frequently erupt lingual to their deciduous counterparts and move forward under the influence of tongue pressure as they erupt. The maxillary central incisors appear as large bulges in the mucobuccal vestibule above the deciduous incisors before they erupt. Calendric age is even less reliable as a bases for projection of eruption of maxillary and mandibular

incisors.

More

sophisticated research and the accumulation

of

precise

developmental data from several “growth centres” has indicated that the physiologic age provides a better yard stick. Those neat and simplified “tooth eruption charts” based on specific ages, posted in schools, physicians offices etc. with no indication of range, standard deviation or standard error

provide

little

useful

information. By themselves, these charts are often misleading and can delude an inquiring parent into a sense of false security.

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The period from eruption of the lateral incisors to the eruption of canine is termed by Broadbent as the “ugly duckling stage”. It is an apt term, implying an unaesthetic metamorphosis leading to an esthetic result. During this period parents become worried. A space may develop between the maxillary central crowns. The lateral crowns may flare. Frenums are often sacrificed in an effort to remove the cause of the space between the centrals.

Actually, the crowns of the cuspids in the young jaw impinge as the developing roots of the lateral incisors, driving the roots medially and causing the crowns to flare laterally. The roots of the centrals are also forced towards each other. As the laterals erupt further, narrower portions of their roots are in proximity to the developing canines. Margolis has called the alveolar process “the servant of the tooth”. At this stage the maxilla is bulging in the canine region as the alveolar process develops around the forming canine. With the further migration of the canine occlusally, with its servant the alveolar process, the point of influence of the canine on the laterals shifts incisally so that eventually, the lateral crowns are driven medially, also effecting closure of the space between the centrals. Eruption of the incisors is usually completed by eight and a half years of age. Even though the central and lateral incisors erupt into the normal position, root formation is not complete. The apices are wide open and do not close for at least another year. Between nine and ten years of age, the apices in the

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deciduous canines and molars begin to resorb. Individual variation is great here. Girls are usually a year to a year and a half ahead of boys. After Ten Years Between 10 and 12 years of age, there is considerable variability in the sequence of eruption of the canines and premolars. In about half the cases, the mandibular canines erupt ahead of the mandibular first and second premolars. In the maxilla, the first premolar usually erupts before the canine. The first premolar usually erupts before the canine. The maxillary second premolar and the maxillary canine erupt at about the same time. At times, deciduous teeth are retained beyond the time that they should normally be shed. A good rule of thumb is to try and maintain the left and right sides on approximately the same schedule. If the upper left deciduous molar is lost naturally and the upper right first deciduous molar is still firm, radiographic evidence may show that the mesial or distal root has not resorbed properly. It is then advisable to assist the removal of the tooth. Eruption of the second molar teeth usually occur shortly after the appearance of the second premolars. Since the second premolar and second molar teeth show the greatest variability in order of eruption of any of the teeth (third molars excepted), the second molar teeth may be expected to erupt before the second premolar teeth in 17% of cases in Caucasians. Both maxillary and mandibular second molars erupt at about the same time. Here again, we are confronted with the raising of the bite that is the gingival pads overlying the upper second molars contact prematurely, blocking open the bite anteriorly allowing eruption of teeth anterior to second molar, for a couple of weeks.

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If the second molars exfoliate before the second premolars, occasionally the first permanent molars may tip to the mesial. This is especially true in patients with premature loss of second deciduous molars. If the molars are tipped mesially, the eruption of the second premolar is further delayed, it may erupt lingually or may not erupt at all. Radiographs taken shortly after eruption of second molar teeth often show an image of the developing third molar teeth that are difficult to interpret. This is especially true of the mandibular third molars. Since the alveolar process curves lingually at the point of juncture with the anterior border of the ramus, the 3rd molars (which are seen to be in the ramus but actually present lingual to the ramus) may erupt lingually. Although maxillary second molars erupt in a downward and forward direction, the maxillary third molars erupt downward and backwards. To this might be added the term ‘outward’. It is not possible to estimate a definite time of eruption of third molars. Hume estimates the median time of eruption of 20.5 yrs. Eruption of 3rd molars is seen more rapidly in girls than in boys. By 20 yrs of age must females have their 3rd molars if they have going to have them. This is not true for males.

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It is easy to understand that problems arise frequently in the third molar area considering the initial deficiency in arch length, the tendencies for the maxillary and mandibular molars to bypass each other, their varying axial inclination and the unpredictable timing of eruption of these teeth. The 3 rd molar problem can be not only be a painful experience but can cause functional disturbance which can affect longevity of the dentition and create and aggravate TMJ pathology. Chronology of the human dentition Teeth

Hard tissue formation begins

Amount of enamel formed at birth

Enamel completed

Eruption

Root completed

Deciduous dentition Maxillary Central incisor Lateral incisor Cuspid First molar Second molar

4 mo in utero 4 ½ mo in utero 5 mo in utero 5 mo in utero 6 mo in utero

Five sixths Two thirds One third Cusps united Cusp tips still isolated

1 ½ mo 2 ½ mo 9 mo 6 mo 11 mo

7 ½ mo 9 mo 18 mo 14 mo 24 mo

1 ½ yr 2 yr 3 ¼ yr 2 ½ yr 3 yr

Mandibular Central incisor Lateral incisor Cuspid First molar Second molar

4 ½ mo in utero 4 ½ mo in utero 5 mo in utero 5 mo in utero 6 mo in utero

Three fifths Three fifths One third Cusps united Cusp tips still isolated

2 ½ mo 3 mo 9 mo 5 ½ mo 10 mo

6 mo 7 mo 16 mo 12 mo 20 mo

1 ½ yr 1 ½ yr 3 ¼ yr 2 ¼ yr 3 yr

Permanent dentition Maxillary Central incisor Lateral incisor Cuspid First bicuspid Second bicuspid First molar Second molar Third molar

3-4 mo 10-12 mo 4-5 mo 1 ½ - 1 ¼ yr 2-2 ¼ yr At birth 2 ½ - 3 yr 7-9 yr

4-5 yr 4-5 yr 6-7 yr 5-6 yr 6-7 yr 2 ½ - 3 yr 7-8 yr 12-16 yr

7-8 yr 8-9 yr 11-12 yr 10-11 yr 10-12 yr 6-7 yr 12-13 yr 17-21 yr

10 yr 11 yr 13-15 yr 12-13 yr 12-14 yr 9-10 yr 14-16 yr 18-25 yr

Mandibular Central incisor Lateral incisor Cuspid First bicuspid Second bicuspid First molar Second molar Third molar

3-4 mo 3-4 mo 4-5 mo 1 ¼-2 yr 2 ¼ - 1 ½ yr At birth 2 ½-3 yr 8-10 yr

4-5 yr 4-5 yr 6-7 yr 5-6 yr 6-7 yr 2 ½-3 yr 7-8 yr 12-16 yr

6-7 yr 7-8 yr 9-10 yr 10-12 yr 11-12 yr 6-7 yr 11-13 yr 17-21 yr

9 yr 10 yr 12-14 yr 12-13 yr 13-14 yr 9-10 yr 14-15 yr 18-25 yr

Sometimes a trace

Sometimes a trace

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V. ACTIVE AND PASSIVE ERUPTION According to the concept of continuous eruption (Orbans, Gottlieb J. Dent. Res. 13 ; 214 ; 1933), eruption does not cease when the teeth meet their functional antagonists but continues throughout life. It consists of an active and passive phase. Active eruption – is the movement of the teeth in the direction of the occlusal plane. Passive eruption – is the exposure of the teeth by the apical migration of the gingiva. This concept distinguishes between the: Anatomic crown - the portion of the tooth covered by enamel. Anatomic root - the portion of tooth covered by cementum. Clinical crown - the part of the tooth that has been derived of its gingiva and projects into the oral cavity. Clinical root - that portion of the tooth covered by periodontal tissues. When the teeth reach their functional antagonists, the gingival sulcus and junctional epithelium are still on the enamel, and the clinical crown is approximately two thirds of the anatomic crown. Active and passive eruption were believed by Gottlieb to proceed together. Active eruption is coordinated with attrition. The teeth erupt to compensate for tooth substance worn away by attrition. Attrition reduces the clinical crown and prevents it from being disproportionately long in relation to the clinical root, thus avoiding excess leverage in the periodontal tissues.

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Ideally, the rate of active eruption keeps pace with tooth wear, preserving the vertical dimension of the dentition. As the teeth erupt, cementum is deposited at the apices and furcations of the roots, and bone is formed along the fundus of the alveolus and at the crest of the alveolar bone. In this way, part of the tooth substance lost by attrition is replaced by lengthening of the root and socket depth is maintained to support the root. Passive eruption is divided into four stages. Although this was originally thought to be a normal physiologic process, it is currently considered a pathologic process. 1. Stage one:

The teeth reach the line of occlusion. The junctional epithelium and the base of the gingival sulcus are one the enamel.

2. Stage two:

The junctional epithelium proliferates so that part is on the enamel. The base of the sulcus is still on the enamel.

3. Stage three:

The entire junctional epithelium is on the cementum, and the base of the sulcus is at the cementoenamel junction. As the junctional epithelium proliferates from the crown onto the root, it remains at the CEJ no longer than any other area on the tooth.

4. Stage four:

The junctional epithelium has proliferated further on the cementum. The base of the sulcus is on the cementum, a 27


portion of which is exposed. Proliferation of the junctional epithelium onto the root is accompanied by degeneration of gingival and periodontal ligament fibres and thin detachment from the tooth. The cause of this degeneration is not understood. At present however, it is believed to be the result of chronic inflammation and therefore a pathologic process. The distance between the apical end of the junctional epithelium and the crest of the alveolus remains constant throughout continuous tooth eruption (1.07mm). Exposure of the tooth by the apical migration of the gingiva is called gingival recession or atrophy. According to the concept of continuous eruption, the gingival sulcus may be located on the crown, CEJ, or root depending on the age of the patient and the stage of eruption. Therefore some root exposure with age is considered normal and referred to as physiologic recession. As mentioned previously, this concept is not accepted at present. Excessive exposure is termed pathologic recession.

VI. SHEDDING OF DECIDUOUS TEETH The physiologic process resulting in the elimination of the deciduous dentition is called shedding or exfoliation. The eruptive pathway of the permanent teeth is very much related to the shedding or exfoliation of the deciduous teeth as pressure from the erupting successional tooth helps to determine the pattern of deciduous tooth resorption. Shedding of teeth can occur due to two factors: 1)

Odontoclasts.

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The resorption of the hard tissues of the tooth is achieved by cells that have an identical histology to osteoclasts but which, because they are involved in the removal of dental tissue, are sometimes called odontoclasts. The odontoclasts are capable of resorbing all dental hard tissues, including enamel, but it is most commonly found on the surface of roots, where it resorbs cementum and dentin. It is also found on occasion within the pulp chamber, resorbing coronal dentin. This variation in the pattern of the deciduous tooth resorption depends very much on the position of the successional tooth in relation to the deciduous tooth. Thus, since the permanent incisors and canine develop lingually to the deciduous teeth and erupt in an occlusal and vestibular direction, resorption occurs at the lingual surface of the root and the tooth is shed with much of its pulp chamber intact. Permanent premolars, however, develop between the divergent roots of the deciduous molars and erupt in an occlusal direction. Hence the resorption of the with interradicular dentin occurs with the resorption of the pulp chamber and coronal dentin. While little is known about resorption of the dental hard tissues, even less is known about the resorption of the soft tissues associated with them; such as dental pulp and periodontal ligament. Simple observation of histological sections shows that the loss of periodontal ligament is abrupt. Electron microscopic examination confirms this finding and also shows that cell death occurs in this region in the absence of inflammation. 2)

Pressure Obviously, pressure from the erupting successional tooth plays a role in

the shedding of the deciduous dentition. For instance, if a successional tooth germ is congenitally missing or occupies an aberrant position in the jaw,

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shedding of the deciduous tooth is delayed. Yet the tooth is eventually shed. Growth of the jaws and also the muscles of mastication also aid in resorption of deciduous teeth. Pattern of shedding It has been seen that the pattern of exfoliation is symmetrical for the right and left sides of the mouth. Girls exfoliate their teeth before boys. The greatest discrepancy between the sexes is observed for the mandibular canines, the least for the maxillary central incisors. Clinically it has been noticed that human deciduous teeth are shed with little bleeding, when the teeth naturally exfoliate. Immediately after teeth are shed, stratified squamous epithelium present in the dentogingival junction (DGJ) and gingiva were found in the underlying tissue indicating that DGJ epithelium and gingival epithelium play an important role in the process of exfoliation. Furthermore, wound healing after exfoliation is usually more rapid than after eruption. A study by N. Sahara et al. showed migration appeared to be further stimulated as a result of chronic inflammation by microorganisms present adjacent to the DGJ. The most interesting finding of the study was the evidence of the stratified squamous epithelium of the DGJ and gingiva proliferated and migrated towards the inside of the crown and eventually ended up under the deciduous crown.

VII. CLINICAL SIGNIFICANCE 1.

Caries during Tooth Eruption (Particularly in First Molars) Caries is a disease with many causal factors. It is known to occur very

often in the occlusal surfaces of the first molars. The risk of caries is highest during the first two years after the eruption of the first molars (i.e. the first

30


molars’ first two years), which roughly corresponds to the one to three year period during which the first molars complete their eruption. Survey studies revealed that, during the first 12 months after the first molars had started erupting, caries was found on 6% of the maxillary first molars and almost 20% of the mandibular first molars. During the first 24 months this percentage jumped to 37% of the maxillary first molars and 62% of mandibular first molars. The four major types of caries causal factors are: a.

The susceptible tooth.

b.

Cariogenic bacteria in plaque.

c.

Substrates.

d.

Time (long term accumulation of plaque etc.)

Let us briefly examine each of these 4 factors: a. Susceptible tooth : susceptibility to caries is largely determined by hereditary and environmental factors, and in the first molars is also caused by such anatomical factors as the large occlusal surface and the numerous deep sulci, grooves and fissures. In addition, a long period is required for eruption and during this period, the tooth substance is still young. b. Cariogenic bacteria are also part of oral microbiota. Cariogenic bacteria known to the present time are Streptococcus Mutans, Streptococcus Sanguis, Lactobacillus Acidophilus, Actinomyces Viscosus and Actinomyces Naeslundii.

31


c. Substrate (glucides) : adherence of plaque to teeth is a natural consequence of the teeths’ role in eating. d. Time : two temporal factors contribute to tooth decay. These are: i. ii.

the time since eruption in which the teeth lay exposed in the mouth. the period of time that elapses before the plaque is removed.

Therefore, the environment most conducive to rapid outbreak of caries is that found during the first molars eruption period. However, when just about two thirds of occlusal surface has erupted, in the 1st and 2nd molars, although gingiva still covers the crown edges which makes them extremely conducive to decay and difficult to clean. Caries occur quite easily during this stage and utmost caution must be taken to achieve adequate oral hygiene. This can be achieved by fluoride treatment and use of molar brushes. It is also common for caries in primary second molars and in neighbouring primary teeth, to spread to the permanent first molar, which then leads to problems in the entire permanent dental arch. Therefore, it is very important to protect the primary teeth from caries thereby allowing the permanent to develop and erupt normally. 2. It is evident that the principal supporting tissue of the tooth, the periodontal ligament and the bone of the jaw, possess a remarkable plasticity that enable the tooth to react favourably or unfavourably to its immediate environment. This plasticity of the supporting tissue is used by the orthodontist to achieve a favourable clinical response. By applying forces to the tooth and by relying on the biologic responses of bone and periodontal ligament, malalignment of teeth can often be corrected.

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3. Sometimes when trauma occurs to the tooth especially permanent anteriors, before the root formation is complete, it results in the formation of blunderbuss canals. At this time endodontic therapy namely apexification or apexogenesis is advocated to stimulate completion form of root apex. 4. Premature eruption of teeth occurs infrequently. Sometimes, infants are born with “erupted� lower central incisors, but this is an example of gross maldevelopment. Such teeth need to be extracted as soon as possible because they prevent suckling. Premature loss of a deciduous tooth without closure of the gap may lead to early eruption of its successor. 5.

Far more common, however is the occurrence of delayed or retarded eruption. This may be caused by localized or systemic factors. Systemic factors include nutritional, genetic and endocrine deficiencies. Local factors include, such situations as loss of a deciduous tooth and drifting of opposing teeth to block eruptive pathways. Severe trauma may eliminate the dental follicle and hence periodontal ligament formation is prevented. When this happens, the bone of the jaw fuses with the tooth, a condition known as ankylosis, and eruption is not possible.

6.

Whites exhibit an evolutionary trend to a diminution in the size of the jaws. This trend has not been accompanied by a corresponding decrease in size of teeth and as a result crowding is a common occurrence. The third molars are the last teeth to erupt and frequently all the available space has been used. And as a result teeth become impacted. Canines are also often impacted because of their late eruption time.

7.

Finally, it has been shown that the moment a tooth breaks through the oral epithelium, an acute inflammatory response occurs in the connective

33


tissue adjacent to the tooth. This is seen even in the germ-free animals and is seen in varying degrees around all teeth throughout life. Clinically, as teeth break through the oral mucosa, there is often some pain, slight fever and general malaise, all signs of an inflammatory process. In infants, these symptoms are popularly called “teething�.

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VIII. SUMMARY & CONCLUSION The mechanism of tooth eruption is an enigma which has perplexed many investigators. It is a process that has been the subject of scientific enquiry since 1778 when Hunter attributed the mechanism to root elongation. Recent reviews have concluded that there is no simple explanation for this biological phenomenon which is not surprising since most teeth erupt during periods of active craniofacial growth and therefore eruption should be considered as part of a multifactorial event. Furthermore, some evidence suggests that different mechanisms operate during various stages of eruption and for teeth which have limited or continuous growth. Recent advances in biochemistry, immunology and structural and molecular biology have renewed interest in understanding the mechanisms of bone remodeling and tooth eruption because it is now possible to localize and determine the activity of cytokines, membrane receptors, signal transduction molecules and post activation intracellular events.

IX. REFERENCES 1.

Eruption of Permanent Teeth – A Colour Atlas – Sadakatsu Sato and Patricia Parsons (Ishiyaku Euro America Inc.).

2. 3.

Oral Histology – A.R. Ten Cate, Mosby Publications (3rd edition). Orban’s Oral Histology and Embryology – Mosby Publications (10th edition).

4.

Principles of Anatomy and Oral Anatomy for Dental Students – M.E. Atkinson and F.H. White (1st edition) Churchill Livingstone Publishers.

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Orthodontics, Principles and Practice - T.M. Graber (3 rd edition)

5.

W.B. Saunders Publication. Clinical Periodontology - Carranza and Newman (8 th edition)

6.

W.B. Saunders Publication. Journals 1. Mechanism of tooth eruption – T.B. Kandos. B.D.J. Vol. 181, No. 3 Aug. 10 : 1996 (91-95). 2. Tooth eruption and orthodontic movements – J.R. Sandy. B.D.J. Vol 172, No. 4 : Feb 22, 1992 (141-149). The Molecular Biology of Initiation of Tooth Eruption - G.E. Wise and F Lin. J. Dent. Res. 74 (1) : 303-306 Jan 95. 3. –

A Histologic study of the Exfoliation of Human Deciduous Teeth N. Sahara, N. Okafuji, Y. Ashizawa and K. Suzuki.

J. Dent. Res. 72 (3) : 634-640, March 93.

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Eruption of teeth/ dental implant courses by Indian dental academy