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Introduction Definition Theories of eruption Anatomic stages in the eruption of the teeth Nollas stages of tooth development Patterns of tooth movement Shedding of teeth Sequence of tooth eruption Molecular determinants of tooth eruption Teeth and teething difficulties Management of teething Problems in primary tooth eruption
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The word eruption properly refers to the cutting of the tooth through the gum. It is derived from the Latin word Erumpere, meaning The Breaking Out. It can also be interpreted as eruption means the axial or occlusal movement of the tooth form its

development position in occlusal plane.

Maury Massler and Schour (1941) : Eruption is a process whereby the forming tooth migrates from its intraosseous location in the jaws to its functional position within the oral cavity. Osborne : Eruptive movement is defined as the axial movement of the tooth which brings the crown of

the tooth from its developmental position within the bone of the jaw to its functional position within the oral cavity.

James K Avery : Eruption is the movement of the teeth from the bone of the jaws and the overlying mucosa to appear and function in the oral cavity.

 There are many theories that explain the mechanism of tooth eruption:

1. 2. 3. 4. 5. 6. 7. 8.

VASCULARITY THEORY PRESSURE THEORY/ CELLULAR PROLIFERATION THEORY ROOT FORMATION THEORY/ ROOT ELONGATION THEORY BONE REMODELLING THEORY DENTAL FOLLICE THEORY PERIODONTAL LIGAMENT THEORY/ GROWTH OF PERIODONTAL TISSUES FORCE THEORY / PRESSURE FROM MUSCULAR ACTION HYDROSTATIC PRESSURE THEORY/ BLOOD PRESSURE THRUST THEORY
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9. 10. 11. 12. 13.

PULPAL CONSTRICTION THEORY PERIODONTAL LIGAMENT CONTRACTION THEORY RESORPTION OF THE ALVEOLAR CREST HORMONAL THEORY FOREIGN BODY THEORY

1. Vascularity
Vascularity plays an important role in tooth eruption Sufficient blood supply to the tooth germ has proven to cause eruptive tooth movement Localized hyperaemia has shown to causes increased vascularity of the periodontal tissue and also increased eruption of adjacent tooth. Evidence for the theory- Submerged teeth often erupt under the influence of hyperaemia, the hyperaemia in periodontitis causes a supra-eruption of teeth.

2. Pressure / Cellular Proliferation Theory

Decreased pressure overlying a tooth and increased pressure around the tooth are major factors in tooth eruption. When the root formation begins an eruption pathway develops overlying the tooth, just like a growing plant. Remodelling of tissue around the developing tooth brings about an increase in pressure tooth which causes the tooth movement.

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3. Root formation

Root formation causes an overall increase in the length of the tooth.

It produces enough force that leads to the resorption of bone. However, this force in itself does not cause tooth movement. Evidence against the theory - Rootless teeth also erupt. One point of importance is that, the tissue beneath the growing root resists the apical movement of the developing root. This resistance results in the occlusal movement of the tooth crown as the root lengthens.

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4.Bone remodelling
The selective resorption and formation of bone surrounding the tooth cause its movement.
This theory also explains the tooth movement during pre-eruptive phase. Bone formation also occurs apical to the developing tooth

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5. Dental Follicle

There is signalling between the reduced enamel epithelium and the dental follicle.
This signalling regulates the timing of eruption of teeth known as biologic clock. By providing a signal and chemo attractant for osteoclasts, it is possible that the dental follicle can initiate bone remodeling which goes with tooth eruption. Teeth eruption is delayed or absent in animal models and human diseases that cause a defect in osteoclasts differentiation.

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6. Periodontal ligament The remodelling of PDL has also been considered as a factor for tooth eruption. The fibroblasts possess traction power that causes tooth movement. The PDL helps lift the tooth to its occlusal plane during the supraosseous phase of eruption

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PDL

Root

Bone

Force theory
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7. Force theory / Pressure from Muscular Action

Berten suggested that the action of the musculature of the cheeks and lips upon the alveolar process might serve to squeeze the crown of the tooth out into the oral cavity like a pumpkin seed from between the fingers

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8. Hydrostatic Pressure
A number of studies exist to demonstrate that there is a hydrostatic pressure difference between the tissue around the erupting crown and its apical extent The hydrostatic theory was investigated by Hassel and McMinn (1972) who demonstrated that the tissue pressure apically was greater than occlusally theoretically generating an eruptive force. No association was found between the rate of eruption and the pressure gradient. Modification of the pressure changed the rate of eruption in rabbits which somewhat supported the theory.

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9. PULPAL CONSTRICTION
This theory states that the growth of the root dentin and the subsequent constriction of the pulp may cause sufficient pressure to move the tooth occlusally. Evidence for the theory- The pulp is progressively constricted by growth of root dentin Evidence against the theory - Pulpless teeth erupts at the same rate as the normal teeth, premolar will often jump into occlusion after the premature extraction of the deciduous molar without any appreciable growth of dentine or pulpal constriction.

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10. PERIODONTAL LIGAMENT CONTRACTION THEORY

Suggests that the contractile element within the periodontal ligament, collagen constriction due to fibroblasts are responsible. Evidence to this theory - The actual force required to move the tooth is linked to the contractility of fibroblasts. When fibroblasts are plated onto silicone rubber, they crawl about and doing so create wrinkles or folds in the rubber indicating that tractions forces are associated with locomotion.

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11. RESORPTION OF ALVEOLAR CREST THEORY

Resorption of the alveolar crest would serve to expose the crown of the tooth into the oral cavity. This theory is not tenable since histological examination shows that the alveolar crest is the site of the most rapid and continuous growth of bone.

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12. HORMONAL THEORY

Sir Arthur Keith suggested that the hormones secreted by the thyroids and pituitary glands might govern the eruption of the teeth. This theory does not attempt to explain the mechanism of the eruption of the teeth, and only points out the fact the hormones may affect the eruption of the teeth.

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13. FOREIGN BODY THEORY

Gottliebs foreign body theory, states that a calcified body such as the tooth tends to be exfoliated by the tissues just as does any foreign body.

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Given by Noyes and Schour : Stage I : Preparatory stage (opening of the bone crypt) Stage II: Migration of the tooth toward the oral epithelium Stage III: Emergence of crown tip into the oral cavity. (Beginning of clinical eruption) Stage IV: First occlusal contact

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Phase 1: The Pre-eruptive phase

Phase 2: The Pre-functional eruptive or eruptive phase

Phase 3: The Functional eruptive or post eruptive phase

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Pre-Eruptive Phase
All movements of primary and permanent tooth crowns from the time of their early initiation and formation to the time of crown completion. Eccentric growth is accompanied with bone resorption altering the shape of the crypt The phase is finished with early initiation of root formation. Early in the stage, the permanent anterior teeth begin developing lingual to the incisal level of the primary teeth. Later, as the primary teeth erupt, the secondary teeth are positioned lingual to the apical third of their roots. Permanent premolars shift from a location near the occlusal area of the primary molars to a location enclosed within the roots of the primary molars
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Permanent molars have no predecessors

Maxillary molars develop within the maxillary tuberosity with their occlusal surfaces slanted distally Mandibular molars develop in the ramus with the occlusal surfaces slanting mesially

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Pre-eruptive tooth movement: Why do developing crowns move constantly in the jaws during the pre-eruptive phase? To place teeth in position for eruptive tooth movement 1.To alleviate the problems of jaw growth which allows second molar to move backward and anterior teeth to move forward 2.Developing crown move constantly during the pre-eruptive phase as they respond to positional changes of the neighboring crowns and to changes in the mandible and maxilla

3.Permanent teeth develop lingual to the incisal level of the primary anterior teeth and later as primary teeth erupt, the permanent crowns are lingual to the apical 3rd of primary roots
4.Permanent premolars move from occlusal level of primary molars to a position enclosed within the primary tooth roots 5.All movements in the preruptive phase occur within the crypts of the developing crowns
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Two types of tooth movement in pre-eruptive phase:

1.

Total bodily movement

2.

Movement where one part remains fixed while the rest continues to grow leading to change in the center of the tooth germ

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Figure from Ten Cates Oral Histology, Ed., Antonio Nanci, 6th edition

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Pre-Functional Eruptive
Starts with the initiation of root formation and ends when the teeth reach occlusal contact Four major events occur during this phase: 1. 2. 3. Root formation Movement occurs incisally or occlusally through the bony crypt to reach the oral mucosa Penetration of the tooth crown tip into the oral cavity

4.

Intraoral movement occlusally and incisally until clinical contact with the opposing crown occurs.

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Eruptive Tooth Movement 4 major events occur: 1. Root formation. Space is required for root formation Proliferation of epithelial root sheath Initiation of root dentin and pulp Increase in fibrous tissue of the follicle 2. Movement. Occurs incisally or occlusally The main reason for movement is so that the roots can form normally Reduced enamel epithelium fuses and contacts the oral epithelium 3. Penetration of the tooths crown tip through the fused epithelial layers allowing entrance of the crown into the oral cavity 4. Intraoral incisal or occlusal movement of the erupting tooth continues until clinical contact with the opposing crown occurs
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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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Clinical crown: During eruption, the exposed crown extending from the cusp tip to the area of the gingival attachment Anatomic crown: Entire crown, extending from cusp tip to the cementoenamel (CE) junction

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Degeneration of connective tissue (decrease in blood vessels and degeneration of nerves) immediately overlying the erupting teeth

Histology changes that occur in tissues overlying erupting teeth

Eruption pathway altered tissue area overlying the teeth

Macrophages destroy cells and fibers by secreting hydrolytic enzymes Gubernacular cord: The connective tissue overlying a successional tooth that connects with the lamina propria of the oral mucosa by means of a strand of fibrous connective tissue that contains remnants of dental lamina Gubernacular canal: Holes noted in a dry skull noted lingual to primary teeth in jaws that represent openings of Gubernacular cord As the successional teeth erupt, Gubernacular canal widens enabling tooth to erupt
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Essentials of Oral Histology and Embryology. James Avery, 2nd edition Figure from Ten Cates Oral Histology, Ed., Antonio Nanci, 6th edition

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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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Figure from Ten Cates Oral Histology, Ed., Antonio Nanci, 6th edition

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Stages of tooth eruption

Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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Histology Surrounding tissues

The surrounding fibers change from being parallel to the tooth surface to bundles that are attached to the tooth surface and extending towards the periodontium (bone) The periodontal ligament have contractile properties and changes drastically during eruption

During eruption, collagen fiber formation and turnover are rapid enabling fibers to attach and release and attach in rapid succession.
Some fibers may attach and reattach later while the tooth moves occlusally as new bone forms around it and the fibers will organize and increase in number and density as the tooth erupts

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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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The rate of tooth eruption depends on the phase of movement Intraosseous phase: 1 to 10 m/day Extra osseous phase: 75 m/day

Environmental factors affecting the final position of the tooth: Muscular forces Thumb-sucking

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Functional Eruptive Phase

1. 2. Movements to accommodate the growing jaws. Mostly occurs between 14 and 18 years by formation of new bone at the alveolar crest and base of socket to keep pace wit increasing height of jaws. Movements to compensate for continued occlusal wear. Compensation primarily occurs by continuous deposition of cementum around the apex of the tooth. However, this deposition occurs only after tooth moves. Similar to eruptive tooth movement. Movements to accommodate interproximal wear. Compensated by mesial or approximal drift. Mesial drift is the lateral bodily movement of teeth on both sides of the mouth. Very important in orthodontics.

3.

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Several factors control mesial drift:

(a) Contraction of the transseptal fibers: As the proximal tooth surfaces of adjacent teeth become worn from functional tooth movement, the transseptal fibers of the periodontal ligament become shorter (due to contraction) and thereby maintain tooth contact. (b) Adaptability of bone tissue: The side of pressure on PDL fibers causes bone resorption, whereas pull on the fibers causes bone apposition (formation). Therefore, as the contact areas of the crowns wear, the teeth tend to move mesially, thereby maintaining contact (c) Anterior compartment of occlusal force: An anteriorly directed force is generated when teeth are clenched, due to the mesial inclination of most teeth and the forward-directed force generated from intercuspal forces. Eliminating opposing teeth results in elimination of biting forces, causing a slowing down of the mesial migration (d) Pressure from soft tissues: Buccal mucosa and tongue push teeth mesially
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Active eruption: to compensate incisal and occlusal wear Passive eruption: gradual recession of the gingiva and the underlying alveolar bone Both active and passive eruption leads to lengthening of clinical crown

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Shedding of Teeth 1. 2. 3. Osteoclast/bone remodeling Odontoclast (cementoclast; dentinoclast) Resorption of soft tissues

Pressure from successional teeth

Odontoclast

Figure Source: Dr. Sandra Meyers

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Osteoclasts are bone resorbing cells derived form monocyte- macrophage lineage Giant multinuclear cells with 4-20 nuclei Osteoclasts resorb hard tissue by separating mineral from the collagen matrix through the action of hydrolytic enzymes Resorption occurs at the ruffled border which greatly increases the surface area of the Osteoclast in contact with bone

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Shedding of Mandibular incisor

5 months

At birth

1 year

2 years
Figure Source: Dr. Sandra Meyers

3.5 years

4.5 years
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Deciduous 1st molar

Figure from Ten Cates Oral Histology, Ed., Antonio Nanci, 6th edition

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Shed element following shedding of primary incisor

Complete resorption of roots Resorption lacunae seen (arrow) Most of coronal pulp is intact

Figure Source: Dr. Sandra Meyers

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7 years-functional occlusion attained but root apex is still not fully formed

15 years incisal wear

Figure Source: Dr. Sandra Meyers
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Sequence and chronology of tooth eruption

Source: http://www.columbia.edu/itc/hs/dental/d9903/lectures/lecture4.pdf 60

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The six/four rule for primary tooth emergence Four teeth emerge for each 6 months of age
1. 2. 3. 4. 5. 6 months: 4 teeth (lower centrals & upper centrals) 12 months: 8 teeth (1. + upper laterals & lower laterals) 18 months: 12 teeth (2. + upper 1st molars & lower 1st molars) 24 months: 16 teeth (3. + upper canines & lower canines) 30 months: 20 teeth (4. + lower 2nd molars & upper 2nd molars)

Summary
1. 2. 3. 4. By 5 months in utero, all crowns started calcification By 1 year old, all crowns completed formation By 2.5 years, all primary teeth erupted By 4 years old, all primary teeth completed root formation

Source: http://www.columbia.edu/itc/hs/dental/d9903/lectures/lecture4.pdf 64

The rules of Fours for permanent tooth development (3rd molars not included)
At birth, four 1st molars have initiated calcification At 4 years of age, all crowns have initiated calcification At 8 years, all crowns are completed At 12 years, all crowns emerge At 16 years, all roots are complete

Source: http://www.columbia.edu/itc/hs/dental/d9903/lectures/lecture4.pdf

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Rules of sixes in dental development

6 weeks old in utero: beginning of dental development 6 months old: emergence of the first primary tooth 6 years old: emergence of first permanent tooth

Source: http://www.columbia.edu/itc/hs/dental/d9903/lectures/lecture4.pdf

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Molecular Determinants of Tooth Eruption

A review article by Wise et al (2002) stated that tooth eruption is a complex and tightly regulated process. Mononuclear cells (Osteoclast precursors) must be recruited into the dental follicle prior to onset of eruption. Recruitment may require colony stimulating factor 1 and monocyte chemotactic protein 1 Parathyroid hormone related protein and interleukin 1 produced in the stellate reticulum are also involved in the signalling pathway

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Control of Eruption
Eruption occurs only during a critical period between 8pm and midnight or 1am. During the morning, tooth eruption ceases or even the tooth intrudes a bit. This reflects Circadian Rhythm reflecting the possible involvement and control of growth hormone and thyroid hormone.

Hormonal Control Mechanisms

A study by Leache et al (1988) of children with growth deficit concluded that children with delayed growth due to growth hormone deficiency or low genetically determined height had delayed tooth eruption. However those with delayed growth for other reasons show normal dental development. This was a large study of children who were shorter than average for their chronological age, although the numbers of children in each group studies were relatively small.
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 The time of eruption for primary and permanent teeth varies greatly. A variation of 6 months on either side of the usual eruption date may be considered normal for a given child.

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Teething and teething difficulties

According to Macknin et al the teething period was defined as the 8-day period beginning 4 days before a tooth emergence and extending 3 days after the event. Over half of babies have one or more problems during teething. In a prospective study by Seward, mothers of 224 infants reported 74% and 100% to suffer at least one local disturbance during the eruption of the front and back teeth, respectively. In the past, a variety of physical disturbances such as croup, diarrhea, fever, convulsions, primary herpetic gingivo-stomatitis, and even death have been incorrectly attributed to eruption. Many of these are common in early childhood, and there is no evidence to support an association with dental eruption . It is now accepted that the localized symptoms of teething vary between individuals, however, severe systemic upsets are unrelated to teething .

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Extra oral & Intraoral symptoms

Finger chewing Lip biting Object biting Irritability/restlessness Night crying Drooling Circumoral rash and inflammation Appetite loss Flushed cheeks Mild temperature elevation Ear rubbing

Gum rubbing Inflammation/gingival redness over erupting tooth Tender swollen gums Tooth erupting

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 Although many studies have suggested associations between teething and a range of signs and symptoms; both local and systemic, the level of evidence remains poor for any causeeffect relationship. Historically, teething has often been blamed when diagnostic ability has failed . Since the eruption of teeth is a normal physiologic process, the association with fever and systemic disturbances is not justified. A fever or respiratory tract infection during this time should be considered coincidental to the eruption process rather than related to it.

Myths and Realities

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 High temperature (higher than 39C) should not be attributed to teething, and should be investigated Since eruption takes place over a period of two and a half years, it is not surprising that these coincidental factors emerge. If attention is given to these symptoms, it is often recognized that some other coincidental mild infection is present, usually gastro-intestinal or upper respiratory. An undiagnosed primary herpetic infection (primary herpetic gingivo-stomatitis) could be responsible for the symptoms of fever, irritability and appetite loss

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 Reassurance of the parents regarding teething signs and symptoms by the pediatrician, dentist or auxiliary staff is necessary. Steward recommended a sequential approach to the management of teething ranging from giving the child objects to bite on through topical and systemic medications. Biting on these chilled objects may give some relief from soreness by the pressure of biting, or hasten the eruption process. Hard vegetables such as chilled carrots or celery may be used. Teething rusks or biscuit preparations are available, consisting mainly of flour or fat. Care should be taken that these do not contain sugar or sweetening

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 If the pain is troublesome, the appropriate dose of paracetamol elixir, preferably sugar-free may be given regularly, every 4-6 hours. Topical medications include gels containing choline salicylate, lidocaine HCl and powders containing benzocaine and paracetamol for temporary relief Uncontrolled application Iatrogenic oral mucosal trauma (chemical burns at the site of application on the mucosa in a 10-month-old boy in Malta) Bonjela, an analgesic drug containing 8.7% choline salicylate in a flavored gel base Choline salicylate is a synthetic non-steroidal anti-inflammatory based on aspirin, Indicated for mild oral and perioral lesions and 1/4-1/2 inch is applied topically 3-hourly, up to a maximum of six applications per day. The drug has a local analgesic effect although the pressure of application may be the true mechanism of action. Less adverse effects when compared to aspirin, however, according to Sarll and Duxbury, it has been reported to cause salicylate intoxication when applied topically in a child. Not believed to be implicated in Reye's syndrome. If topical therapy is required, it must be applied sparingly to localized areas of dry mucosa. The patient must be regularly reviewed and reassessed
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Paediatric Paracetamol Elixir BP Each 5ml contain 120 mg of paracetamol

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 ERUPTION HEMATOMA ERUPTION SEQUESTRUM ECTOPIC ERUPTION NATAL AND NEONATAL TEETH NON ERUPTION OF TEETH LOCAL FACTORS INFLUENCING TOOTH ERUPTION SYSTEMIC FACTORS INFLUENCING TOOTH ERUPTION EARLY EXFOLIATION OF TEETH

AGENESIS OF TEETH

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HYPOPHOSPHATASIA CHERUBISM ACRODYNIA HYPOPHOSPHATEMIA CYCLIC NEUTROPENIA OTHER DISORDERS LIKE: Acatalasia, Chediak-Higashi Syndrome, Coffin Lowry Syndrome, Downs

Syndrome, Ehlers-Danlos Syndrome, Hajdu-Cheney Syndrome, Hyperpituitarism, Hyperthyroidism, Juvennille Diabetes, Papillon-Lefevre Syndrome, Progeria,Singleton-Merten Syndrome, and some mlignant diaseases like Histiocytosis, and Leukemias.

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Eruption hematoma/Eruption cyst

A bluish purple, elevated area of tissue, occasionally develops a few weeks before the eruption

of a primary or permanent tooth. Blood filled cyst mostly associated with primary second molar or first permanent molar ? Trauma during function Self-limiting: usually within a few days, the tooth breaks through the tissues and the hematoma subsides Surgical uncovering

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Eruption Sequestrum
Occasionally occurs at the time of eruption of the permanent molars. Starkey et al. (1963) were the first to report the presence of small fragments of calcified tissue overlying the crowns of erupting molar teeth. Generally, these pieces directly overlay the central occlusal fossa, while remaining within the soft tissue and, as the molar tooth erupts through the bone, a small osseous fragment is lost.

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Ectopic Eruption of First Molars

Ectopic eruption is defined as the abnormal eruption of a permanent tooth out of position

and causing the resorption of a primary tooth in an abnormal fashion.

A disturbance of the path of eruption in a position different to its normal path

In reference to the first molar, the definition is: an ectopic molar erupts at an angle mesial

to the normal path of eruption and atypical resorption of the distal surface of the neighbouring primary second molar.

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Classification
The disorder was first described by Chapman (1923) and later refined by Young (1957) describing two types of ectopic molar eruption:

Jump-Reversible type Hold-Irreversible type

Jump: describes a reversible ectopic eruption typified by a mild manifestation allowing the first permanent molar to free itself from under the second primary molar and erupt into normal position. Account for 66% of cases Hold: describes a permanent molar erupting with a mesial inclination, causing resorption of the primary molar roots such that the first permanent molar becomes trapped under the second primary molar. The tooth will not erupt until treatment is provided or until the primary molar exfoliates causing further mesial tipping, space loss, migration and rotation of the permanent molar

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Aetiology
Remains relatively unknown, however, a number of causes have been suggested: 1. 2. Genetic factors (familial) Imbalance in the growth of the mandible in relation to the eruption of the first permanent molar, which can encourage continued mesial inclination of the molar and subsequent entrapment under the bulge of the second primary molar Arch length deficiency Larger than normal sizes of all maxillary primary and permanent teeth Tendency towards a hypo plastic maxilla Retrusive position of the maxilla in relation to the cranial base Pronounced mesial inclination of the tooth by 15 degrees on average Delayed calcification of the affected molar Improper fit of a SSC on a second primary molar placed prior to eruption of 6 Cleft lip and palate patients following primary palate repair.
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3. 4. 5. 6. 7. 8. 9. 10.

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What are natal and neonatal teeth?

Natal teeth- teeth that are already present at the time of birth. Neonatal teeth- teeth which grow in during the first 30 days after birth. Precocious Dentition- teeth erupting during the 3-5th month of life Normal Dentition -8 months

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85% are the deciduous mandibular incisors

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Location
85% mandibular incisor <.01% lateral mandibular incisor 2.5% other mandibular teeth 4% upper central incisors <.01% other maxillary teeth

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Embryology
Derived from the ectoderm of the first branchial arch, and the ectomesenchyme of the neural crest. For human teeth to have a healthy oral environment, enamel, dentin, cementum, and the periodontium must all develop during appropriate stages of fetal development. Primary (baby) teeth start to form between the sixth and eighth weeks. Permanent teeth begin to form in the twentieth week.

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Embryology
1) Mandible 2) Anlage of the permanent tooth 3) Enamel organ 4) Enamel 5) Dentin 6) Labiogingival sulcus

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Etiology of Natal Teeth also unknown

Unknown. Possible genetic link, as often occurs in same family. No clear genetic pattern has been identified Gates thought it may be an irregular dominant trait, perhaps associated with an inhibitor gene, or the presence of two genes.

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Problems
Natal teeth are usually not well formed, but they are firm enough that, because of their placement, they may cause irritation and injury to the infant's tongue when nursing. Natal teeth may also be uncomfortable for a nursing mother. Riga-Fede

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Solutions
Frequently, natal teeth are removed shortly after birth while the newborn infant is still in the hospital. Must be removed if the tooth is loose and the child runs a risk of aspiration, or "breathing in" the tooth.

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Associations
Most of the time, natal teeth are not related to a medical condition. However, sometimes they may be associated with: Ellis-van Creveld Syndrome Hallermann-Streiff syndrome Jadassohn-Lewandowski Syndrome Sotos syndrome

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1. Ellison van Creveld Syndrome features: Cleft lip and palate Polydactyly Nail problems Short arms and legs Short height (b/w 3.5 5ft) Sparse , absent or fine textures hair Tooth abnormalities : Peg teeth Widely spaced teeth Natal teeth Delayed or missing teeth

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2. Hallerman-Streiff Syndrome : Malformations of skull and facial region Sparse hair Ocular abnormalities Degenerative skin atrophy Short stature Dental changes : Natal teeth Hypodontia or partial anodontia Malocclusion

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3. Jadassohn-Lewandowski Syndrome
Nail disorders Blisters in the different parts of the foot Excessive sweating of the feet Excessive hair growth Thick skin on palms and toes Oral manifestations: Oral mucosal leukoplakia White tongue Natal teeth Premature eruption of primary teeth

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4. Soto's Syndrome Macrocrania Dolicocephaly Prominent forehead Apparent hypertelorism High arched palate Increased birth length and weight Excessive growth in childhood Disproportionately long hands and legs Low muscle tone Developmental delay Expressive language delay Teeth defects like natal teeth

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Summary
Natal teeth are relatively rare (1:3000 births), but you WILL likely see it in your career We dont know what causes it, possibly genetics. Its awesome or scary, depending where you come from. The teeth are usually the lower incisors, and those are the first teeth to erupt normally (8 mo) They are usually premature deciduous teeth and will fall out, they have no roots, and are not well formed. You can pull them out if they are causing mouth ulcers, or pain to mother. They may be associated with syndromes, so a good physical exam is necessary.

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Lingual Eruption of Mandibular Permanent Incisors

Given enough space is present, if labial migration of the permanent incisor had not occurred by 8.2 years for central incisors and 8.4 for lateral incisors, over-retention is suspected and removal of primary teeth is recommended

(Gellin and Haley, 1982)

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Primary Failure of Eruption

Called primary retention, cessation of the tooths movement in the pre-eruptive stage, results in a deeply embedded tooth that fails to achieve emergence and remains covered with a thick layer of alveolar bone. The roots are fully formed and usually unresorbed. In primary teeth 1:10,000, females>males, mostly mandibular primary second molars D/D: secondary failure of eruption (secondary retention, infraocclusion, submergence)

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Aetiology: Genetic Hormonal disturbances Developmental syndrome (Cleidocranial dysplasia) Impaired eruptive process due to abnormal bone resorption, aberrant development of tooth germ, displacement of follicle, physical barrier (considered impaction in this case) Sequelae: Inversion Impaction Management: surgical removal
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Ankylosis
Anatomical fusion of the tooth cementum or dentine to the alveolar bone during or after the active eruption of tooth. It may occur before the emergence into the oral cavity or after the eruption and before they make contact with the opposing teeth. Clinically: tooth below the occlusal level, immobile, dull percussion (high pitch) Radiographically: obliteration of periodontal space and dipped in apically crestal bone

(Teague et al, 1999)

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Source: Color atlas of clinical oral pathology. Neville, Damm and White. 2nd edition

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Aetiology:

Intrinsic: Genetic or congenital gap in the PDL Extrinsic: 1. Local trauma 2. Local metabolic defect 3. Reimplantation 4. Deficient eruptive forces 5. Thermal and chemical insult 6. Facial morphology 7. Forces squeezing the arch 8. Localized infection 9. Abnormal tongue pressure

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Incidence between 8 and 14%, higher among Caucasians and Hispanics Can occur as early as 3 years Mandible> maxilla 10 times more common in primary teeth

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Possible complications: Delayed exfoliation Delayed eruption Malocclusion Tipping Over eruption of opposing tooth Loss of arch length Damage to adjacent teeth (alveolar bone and PDL) Denuded root surface Increase difficulty of extraction Decrease alveolar bone support and increased submergence In severe cases adaptive tongue thrust Retained root fragments
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Submerged primary teeth

Hyper or supra eruption

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Retained Primary teeth

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 Fromm reported that clinically visible cysts were found in 1028 of 1367 newborn infants. He noted and classified the following three types of inclusion cysts: 1. Epstein Pearls are formed along the midpalatine raphe. They are considered remnants of the epithelial tissue trapped along the raphe as the fetus grows. 2. Bohn Nodules are formed along the Buccal and lingual aspects of the dental ridges and on the palate away from the raphe. The nodules are considered as the remnants of mucous gland tissue and are histologically different form Epstein pearls. 3. Dental Lamina Cysts are found on the crest of the maxillary and mandibular dental ridges. The cysts apparently originated form the remnants of the dental lamina

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Systemic conditions causing delayed eruption of teeth

Hereditary gingival fibromatosis Down Syndrome Cleidocranial dysplasia Hypothyroidism Hypopitutarism Achondroplastic dwarfism

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Hereditary gingival fibromatosis

Rare, genetically inherited overgrowth condition A benign fibrous enlargement of maxillary and mandibular keratinized gingival. The gingival enlargement may cover the crowns of teeth and cause severe functional and esthetic concerns. Recurrent even following surgery

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Delayed eruption of both primary and permanent dentitions

Downs Syndrome

35-55% microdontia, clinical crowns are short, conical, small, roots complete

Enamel hypocalcificiation and hypoplasia common

DS patients 50% more likely to have congenitally missing teeth, taurodonts are frequent finding

1/3 more caries resistant than their non-DS siblings

Gingivitis develops earlier and more rapidly and extensively in persons with DS, perhaps because of an abnormality in host defenses. Patients with DS have altered microbiological composition of subgingival plaque, including increased Actinomyces and Hemophilus strains.

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V-shaped palate, incomplete development of the midface complex, soft palate insufficiency Hypotonic O. Oris, Masseter, Zygomatic, Temporalis Muscles Absent incisors make articulation difficult High incidence of laryngeal-tracheal stenosis, also upper airway obstruction and sleep apnea common Scalloped, fissured tongue with bifid uvula, cleft lip/palate, enlarged tonsils/adenoids

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Cleidocranial Dysplasia
Retained primary teeth Delayed eruption of permanent teeth Impaction Abnormal or absent cellular cementum

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Cleidocranial Dysplasia

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Hypothyroidism
Congenital hypothyroidism occurring at birth or during rapid growth period usually causes mental deficiency and dwarfism. The untreated child is usually small and disproportionate person, with abnormally short arms and legs. The dentition is delayed in all stages of eruption.

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The occlusion was normal but with delayed in its development. The maxillary midline supernumerary tooth is coincidental.

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The delayed development in the Juvenile Hypothyroidism patient

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Hypopituitarism
A pronounced deceleration of the growth of the bones and soft tissues of the body will result from a deficiency in secretion of the growth hormone. Delayed eruption of teeth

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Complete primary dentition at the age of 28- years of age

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The roots of the primary teeth have not resorbed to that appreciable degree though some permanent teeth show complete development
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Achondroplastic Dwarfism
Autosomal dominant disorder The maxilla may be small, crowding of the teeth and a tendency for open bite A chronic gingivitis is usually present Development of dentition is usually delayed

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 It implies complete failure of the teeth to develop, a rare condition.

It is often referred to as Congenital absence.

Gorlin and, Herman, and Moss noted that, when agenesis occurs as an isolated trait, the primary dentition is not affected, and the inheritance is normally autosomal recessive. Swallow reported on to an 11-year-old boy who had a complete primary dentition but no permanent dentition. Schneider also observed a 7-year-old white female with primary teeth but with missing permanent teeth.

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Hypodontia (Oligodontia)
Agenesis of some teeth is referred to as Hypodontia, which is preferable to the term Partial Anodontia. Oligodontia is sometimes used when only a few teeth develop. Hypodontia occurs with no known family history, but be found associated with some syndromes, esp. in Ectodermal Dysplasia .

Any of the 32 permanent teeth may be missing. However the most frequent missing in children are the mandibular second premolars, maxillary lateral incisors, and maxillary second premolars .
The absence may be unilateral or bilateral.

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 Glenn observed during an examination of 1702 children that o 5% had a missing permanent tooth other than 3rd molar. o In 97% the formation of 2nd premolar could not be detected radiographically at the age of 5.5yrs and that of the lateral incisor at the age of 3.5 yrs.

Later further studies were done and the causes for the missing tooth/teeth were found : o Mutation in the MSX1 gene located at 4p16.1 o Mutation in the human PAX9 gene o Consanguineous marriage

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Ectodermal Dysplasia
When a no. of the primary teeth fail to develop, other ectodermal deficiencies are usually evident. There are more than 100 types of ectodermal dysplasia with varying anomalies of ectodermal derivatives, including both the primary and permanent teeth, hair nails, and skin. One of the more common types of ectodermal dysplasia is X-linked recessive hypohidrotic ectodermal dysplasia (XLHED), also called as Anhidrotic Ectodermal Dysplasia and Christ-Siemens-Touraine Syndrome. Characteristic features of this are: oHypodontia and dental hypoplasia oHypotrichosis/ Anhidrosis oAsteatosis .

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 Secondary characteristics are: oDeficiency in salivary flow oProtuberant lips oSaddle-nose appearance oDry and scaly skin oFissuring at the corners of the mouth oPrimary teeth maybe of normal or reduced in size oThe primary molars without permanent successors have a tendency to be ankylosed. Development of skeletal structures is normal. Children presenting with this syndrome have normal mental growth and a normal life expectancy. Consanguinity increases the likelihood of expression of a trait or condition that is inherited in a recessive manner, and may be one way that a female with a normal karyotype can be affected.

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Textbook of Pediatric Dentistry - Nikhil Marwah Dentistry for the Child and Adolescent Eighth Edition Ten Cates Oral Histology, Ed., Antonio Nanci, 6th edition Essentials of Oral Histology and Embryology. James Avery, 2nd edition Color atlas of clinical oral pathology. Neville, Damm and White. 2nd edition

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