What makes teeth erupt

Meanwhile, it is known that teeth erupt later in certain syndromes. The condition when teeth are formed in the jaw but do not erupt is rare. It has been described in very few cases and occurs, for example, in GAPO syndrome [ 32 ]. Gapo syndrome is probably an autosomal-recessive condition of growth retardation, alopecia, and optic atrophy [ 32 ].

The cause of this eruption deviation in Gapo syndrome is not known. Local Eruption Deviations. It is characteristic that eruption deviations can occur generally in dentitions as described in the above cases and also locally in single teeth or within tooth groups [ 31 , 33 — 45 ].

Tumours have influenced normal eruption regionally [ 39 , 40 ], and so have supernumerary teeth [ 35 ]. An example of an eruption deviation affecting canines and premolars is described in Hyper IgE syndrome where the primary canines and the primary molars are not shed, while the root formation of the underlying teeth continues to full length [ 17 , 18 , 38 , 42 ]. The cause of regional eruption disturbances associated with alveolar bone malformation may be seen in the jaw fields that have been introduced during recent years based on prenatal studies on cranial and jaw development [ 46 — 50 ].

These fields are demonstrated in Figures 1 — 3 and explained later in the paper. Treatment of regional eruption disturbances is often interdisciplinary [ 51 ]. Eruption deviations also occur as isolated findings in single teeth.

These deviations occur in, for example, the permanent first molar or the second molar [ 52 — 58 ]. Secondary retention of permanent molars occurs after the molar has penetrated the gingival [ 53 ]. The aetiology is not fully understood. Raghoebar et al. It was concluded in that study that the ankylotic areas in several cases could not be detected radiographically [ 57 ].

Barberia-Leache et al. Association between ectopic eruption of maxillary canines and first molars has also been reported [ 55 ]. The explanation for this presumed association has not been given. In the primary dentition eruption arrests are often seen in molars [ 59 , 60 ]. Less severe infraposition of primary molars does not require treatment due to natural exfoliation [ 59 ].

More severe secondary retention of primary molars results in extraction [ 60 ] due to ankylosis. Ectopic Eruption. Every single permanent tooth can erupt ectopically. The prevalence of ectopic eruption is different for individual teeth. Most common in this connection is ectopic eruption of the maxillary canines [ 36 , 61 — 72 ]. The aetiology behind this ectopic condition is intensively discussed. Peck et al. Becker and Chaushu [ 69 ] have in an extended study compared dental ages in patients with bucally displaced canines with a control group with normally located canines.

Approximately half the subjects with palatal displacement exhibited a late-developing dentition while the timing in dental development in the remaining subjects was normal [ 69 ]. Buccal displacement of maxillary canines was not associated with a retarded dental development but demonstrated dental development similar to conditions seen in the control group. This study supports the idea that there are different aetiologies for the occurrence of buccal versus palatine canine ectopia [ 69 ].

It has also been described in the literature that an association exists between palatally ectopic canines and small malformed and missing teeth in the dentition [ 62 , 69 , 70 ]. Sacerdoti and Baccetti [ 71 ] analyzed a sample of subjects and found that the prevalence rate of palatally displaced canines was 2.

Skeletally they reported a reduced vertical relationship in patients with palatally displaced canines. When they in that study [ 71 ] compared unilateral palatally displaced canines with bilateral palatally displaced canine cases they found that unilateral displacement was associated with agenesis of upper lateral incisors whereas bilateral displacement was associated with third molar agenesis [ 71 ].

This is again a finding which has not been explained. This was later confirmed by Artmann et al. Also deviations in the cranio-facio-skeleton have been reported in cases with ectopic maxillary canines [ 63 , 64 ]. Resorption of maxillary lateral incisors due to ectopic eruption of maxillary canines is a severe clinical problem, which is in focus in the literature on ectopic maxillary canines [ 61 ].

Transposition, which is an eruption deviation characterized by the shifting of place in the dental arch of single teeth causing treatment problems, is also a well-known eruption deviation in the permanent dentition [ 73 ]. In these dentitions craniofacial alterations in the maxillary skeleton have also been reported [ 66 ]. This specific type of eruption deviation is seemingly not described in the primary dentition.

Ectopic eruption of other teeth such as mandibular canines and third molars [ 74 , 75 ] is described in the permanent dentition. Transmigration of a mandibular canine is a rare condition with unknown aetiology [ 76 , 77 ].

With regards to aetiology, speculations behind these ectopic eruption courses are many. Most often genetic conditions are defined as the cause of ectopia [ 68 , 75 , 78 ], but that is not always the case.

Ectopia can also be caused by deviations in space that may be hereditary, just as seen in small jaws, but can also be acquired due to early tooth extraction or due to primary teeth that are not shed.

Additionally, a correlation between morphological ectodermal deviations in dentitions and ectopia has been described [ 65 ]. The size, growth, and osseous maturity of the jaw are also parameters that play a role in the understanding of the aetiology behind ectopia [ 64 ]. The space condition and how to analyze space experimentally, especially for third mandibular molar eruption, have been in focus in several reports.

When all these eruption aspects are comprised they provide a good insight into how tooth eruption progresses, when the teeth erupt, and where they erupt, but we have no coherent understanding of why the teeth erupt. When we do not know the aetiology behind eruption and cannot explain the eruption mechanism, then we cannot perform aetiology-based treatment. We can attempt to guess a treatment as, for example, surgical exposure of a first permanent molar that has primarily arrested eruption, because we have experienced that this treatment encourages eruption, but we do not know whether it is the crown follicle or the overlying gingiva, the alveolar bone or perhaps other factors that cause the arrested eruption.

Several reviews from experienced researchers have, like the one from Marks and Schroeder [ 78 ], discussed the mechanism of tooth eruption, which is still not understood.

This review focuses on human and other mammalian teeth with a time- and spacewise limited period of eruption and analyzes recent observations and experimental data on dogs, rats, primates, and humans in a framework of basic biological parameters to formulate a guiding theory of tooth eruption.

Acknowledging basic parameters i. We have critically analysed, summarized, and integrated recent findings associated with preeruptive movements of developing teeth, the intraosseous stage of premolar eruption in dogs, molar eruption in rodents, and premolar and molar eruption in primates.

The variable speeds of eruption are particularly important. In conclusion, the basic principles of tooth eruption depend on the type of signals generated by the dental follicle proper, the conditions under which teeth are moved, and the clinical understanding to be derived from this knowledge. If we look at the explanation and causes presented in the textbooks for the eruption process, we cannot find a clear answer either.

We can read that some authors suggest that the eruption force is connected with the force that occurs when the tooth root grows, that is, suggesting an association between eruption force and root extension [ 79 ]. Other important causes are cell proliferation, increased vascularity, and increased bone formation around the teeth. Additional possible causative agents, which have been noted include: endocrine influence, vascular changes, and enzymatic degradation. Probably all these factors have an influencing role but not necessarily independently of each other.

Although all the factors associated with tooth eruption are not yet known, elongation of the root and modification of the alveolar bone and periodontal ligament are thought the most important factors.

These events are coupled with the changes overlying the tooth that produce the eruption pathway. A connection between pulpal and periodontal reactions has also been mentioned as a causal factor in eruption [ 79 , 80 ].

Each theory for eruption presents a problem in its conception. Root growth, existence of a temporary ligament, vascular pressure, contractile collagen, and hormonal signals genetic targets all have been used to explain eruption.

The dental follicle surrounding the tooth crown has also been described as a factor decisive for the eruption process. One of the most important local environmental factors is crowding among the developing and erupting teeth. Tooth eruption is a biological process, which is still not fully understood. The process is accompanied by multiple tissue changes, such as resorption and apposition of the alveolar bone, and development of the root and periodontium.

The problem is still how the tooth is elevated in the jaw. In general it can be concluded that the individual eruption pattern is inherited, that is, genetic, and that this pattern is also affected by local and general external factors. Many major textbooks do not mention the aetiology behind eruption and some only state that it is unknown [ 79 — 82 ].

Furthermore, Berkowitz et al. Whatever the system implicated in the eruptive mechanism, the evidence should be judged according to the following five criteria. Animal experimental studies support the theory that the follicle is of importance for the eruption process [ 2 , 3 , 83 — 85 ] and have also shown that innervation plays a specific role in tooth eruption [ 4 , 86 — 90 ].

There is no doubt that the bone tissue surrounding the tooth and the general growth conditions in the body play a role [ 21 , 91 — 97 ]. In conditions with abnormal bone such as that observed in osteopetrosis then tooth eruption is affected [ 95 ], but the bone quality is not the only factor, which can explain the eruption process.

Human studies have suggested that there is no convincing correlation between early tooth formation before crown formation evaluated radiographically and the innervation pattern of the jaws [ 98 ].

Even though much is known about several aspects in the human tooth eruption we cannot explain what it is that causes a tooth to move in the jaw after crown formation and gradually erupt, often in a very long eruption path longer than the root of the tooth to its final place in the tooth row.

Considering that the phenomenon of tooth eruption and specifically pathological tooth eruption plays a major role in both clinical and theoretical dentistry there is surprisingly sparse literature on the subject. This is no doubt due to methodological difficulties.

Experimental studies on animal tissue cannot uncritically be transferred to human conditions. Meanwhile, the eruption process cannot be studied on a molecular level sufficiently and furthermore not longitudinally in human tissues because teeth have to be extracted, which separates the teeth from the periodontal membrane and the surrounding bone.

As we cannot understand what causes a tooth to erupt and at the same time claim that the eruption process cannot be studied on animal experimental material and uncritically transferred to humans and secondarily that also human material have its methodological limitations, how can we then form a hypothesis for the eruption process? This proposed hypothesis must be formed based on experience from human material. It is logical to turn to experiences from pathological and genetic material and to analyse what are the consequences of different diseases for different tissue types and for the eruption process.

And then try to gather the information from pathological eruption processes and create a hypothesis for the eruption mechanism. It is not easy, but still it is more difficult based on observations of normal eruption courses to understand, for example, why the permanent first molars erupt at the same time in all four quadrants. It can be registered, but it cannot be explained. Another way to approach the eruption problem is to combine knowledge from histological and histochemical studies of human teeth and jaws from different time before birth with similar studies of teeth including periodontium after birth.

Basic knowledge on tooth tissue and the tissue that surrounds teeth can thus be analyzed in normal foetuses and pathologically genetically deviant foetuses. When this knowledge on tissue and genetics is transferred to the postnatal dentition, a hypothesis can be proposed based on a scientific background. This latter method forms the basis for the presented theory.

Before we try to understand what initiates, moves, lifts, and forms the path for a tooth primordium during eruption it is necessary to look at the early embryonic jaw formation and tooth formation. The mandible and maxilla are formed in the early embryonic developmental stage from neural crest cells.

These cells migrate from different areas on the neural crest of the neural tube with different molecular-biological origin. The cells with the different origins migrate to the different regions, also known as fields, to the jaws [ 49 ]. These fields are schematically marked on a panoramic radiograph, seen in Figure 1. The fields are characterized by having a separate innervation and regionally specific ectomesoderm, which is shown in the regions in Figure 1.

Figure 2 demonstrates the molecular-biological fields in the cranium [ 49 ]. These fields are different not just in the cranium and jaws but also in the dental arches [ 49 ].

The fields have different molecular origins and different innervations. They are shown in the dental arch and palate in Figure 3. The early tooth formation is comprised of an ectodermal epithelial bud surrounded by regionally specific ectomesenchyme [ 48 , 86 , 91 ].

The nerve supply to the early tooth primordium, which is under rapid development, goes through a complicated path-finding process to the tooth primordium and gathers to begin with around the apical part of the primordium [ 91 ]. Quickly, the primordium develops through the well-known cap and bell stages.

During these stages the innervation spreads and surrounds both the apical and the coronal parts of the primordium. Later, the reaction for nerve tissue is seen most strongly apically. The formation and tissue components in the early tooth formation are demonstrated in Figure 4.

The innervation thus comprises a very important tissue component in the apical root sheet or root membrane that could also be designated the root follicle. There is no epithelium in the root follicle in contrast to the follicle around the tooth crown that has a pronounced inner layer of epithelium and only a light outer layer of innervation. In summary, these are thus the tissue types: ectoderm, ectomesenchyme, and nerve tissue that are responsible for the early tooth formation.

The tissue types that influence the early tooth formation are the same tissue types that can be traced in the postnatal tooth formation Figure 5. The crown follicle is comprised of an inner layer of ectoderm and an external layer of cell-dense ectomesenchyme.

The periodontal membrane close to the root is called the peri-root sheet and is comprised of an inner nerve layer covered by a closely knit fibre layer of ectomesenchyme and outermost an ectodermal cell layer Malassez cell layer [ 92 , 99 , ] Figure 6. The apical root sheet or root membrane, suggested to be called the root follicle, is comprised of a strong layer of innervation and of a membrane-like layer of ectomesenchyme.

A tooth that will erupt depends on 1 space in the eruption path, 2 lift or pressure from below, 3 adaptability in the periodontal membrane.

The crown follicle destroys overlying bone tissue and thus creates the necessary space in the eruption path. The molecular-biological processes depend on the ectoderm in the dental follicle and have been thoroughly described in animal experimental studies. The hypothesis is that the root membrane functions as a glandular membrane. The innervation in the membrane [ 91 ] causes, as in the glandular end-cells, an overpressure that supplants to the root surface, periodontal membrane, and pulp tissue [ 88 , ].

To prevent an abnormal eruption and make room for adult teeth, the baby tooth may need to be extracted. Getting teeth pulled can be a scary prospect, but there are ways to make it much easier for you.

This intervention may be very simple — for example a passive appliance to hold space in the arch for the erupting tooth. If you do need braces, technology has come a long way and it may not be necessary to use metal braces and headsets.

Today, you can often choose clear ceramic braces and even invisible aligners. If you had abnormal eruptions as a child that have resulted in bite problems and misaligned teeth, achieving a straighter smile is easier and more affordable than ever before. After a consultation, we can determine the best course of treatment for you and your budget. Anbesol teething gel lidocaine hydrochloride 0. Choline salicylate 8. Lidocaine hydrochloride is rapidly absorbed through mucous membranes, giving rapid, albeit temporary, pain relief [5].

Regarding application, by way of example, around 0. Around 20 minutes should elapse between applications, however, only six applications should be made each day to avoid systemic effects. Systemic analgesics can also be used. Sugar-free paracetamol liquid is the systemic medication of choice for teething infants, given its action in reducing pain and pyrexia. The doses can be repeated at four-hourly to six-hourly intervals, with a maximum of four doses a day [5].

Ibuprofen, which can be given to children aged over one year, is not recommended in the management of teething. Choline salicylate-based products provide analgesia and also have anti-inflammatory and antipyretic effects, which reduce swelling.

The use of salicylates in children is the subject of debate. Many paediatricians and pharmacists advocate the avoidance of choline salicyclate products in teething. For children aged over four months, the recommendation is to gently massage 0. Frequent applications of choline salicylate to the oral mucosa may result in a chemical burn [7]. Adding honey, jam or sugar to a feeding bottle, or dipping a pacifier in a sugary food substance, is to be discouraged.

These remedies have no pain-relieving effect and can cause dental decay and pain. A feeding bottle in bed — in particular one containing a sugary fluid — should also be discouraged, as the teeth are constantly bathed in sugar and, even in low concentrations, this increases the risk of dental decay and subsequent pain and infection.

The application of alcohol to the mucous membrane of an infant should also be discouraged as it has no pain-relieving effect. Teething preparations should be kept out of reach of children to eliminate the chance of overdose.

This could result in the extended retention of your child's baby teeth due to the fact that no permanent teeth dislodge them. Early eruption of adult teeth could result in excessive crowding, and this may make caring for them challenging. These crowded teeth, or any retained baby teeth, may be more susceptible to tooth decay or bite problems as space is tight and limited and food gets stuck quite easily.

In many cases, early eruption is associated with certain types of health conditions. Three of the most common health-related reasons are listed below. If you or other family members have had early adult teeth eruption, then your child is at increased risk for this issue. Also, certain congenital structural jaw problems may cause certain teeth to erupt early. Hyperthyroidism can cause the jaw to grow faster, lead to the early loss of your child's baby teeth, and the early onset of adult teeth.

Alternatively, hypothyroidism can also cause a delay with adult tooth eruption. If your child has lost a tooth through trauma or disease, then the adult tooth can erupt sooner than it would have if that primary tooth wasn't lost, but not always. There are treatments to help with this. The dentist will monitor your child's teeth to determine whether and when any action towards early eruption should take place.

Many times, nothing needs to be done unless the tooth or teeth cause problems such as pain or a bad bite.