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Anatomy and development of the teeth

Anatomy and development of the teeth
Author:
J Tim Wright, DDS, MS
Section Editor:
Ann Griffen, DDS, MS
Deputy Editor:
Diane Blake, MD
Literature review current through: Jan 2024.
This topic last updated: Mar 29, 2022.

INTRODUCTION — The close relationship among oral, systemic, and psychological health requires that oral health be evaluated thoroughly as part of health maintenance supervision. An understanding of the normal sequence and patterns of tooth eruption is the foundation for identifying and treating children with abnormal dental development and optimizing their oral health.

The typical anatomy and development of human dentition are reviewed here. Problems in dental development and syndromes associated with abnormal dental development are discussed separately. (See "Developmental defects of the teeth".)

DENTAL ANATOMY — In addition to their role in speech and facial aesthetics, the teeth provide an efficient system of mastication with incising, tearing, and grinding capabilities. The unique composition and structure of teeth allow them to survive the forces and wear of mastication; alteration of the composition or structure of the teeth affects their durability, resistance to fracture, and retention in the oral cavity.

Each tooth has a visible crown that projects above the gingiva (gum), with one or more roots extending into the alveolar bone of the maxilla or mandible (figure 1). The crown and root meet at the neck of the tooth. The tooth forms a peg and socket joint with the alveolar bone and is held in place by the periodontal ligament that allows slight movement of the tooth.

The four components of teeth are enamel, dentin, pulp, and cementum.

Enamel – Dental enamel is the hardest tissue in the human body; it protects the tooth crown from fracture and wear. The enamel is produced by ameloblasts that secrete, process, and control the mineralization of the unique extracellular matrix. The ameloblasts protect the formed enamel during tooth eruption and then become part of the epithelial attachment of the tooth to the gum [1]. Because the ameloblasts are no longer present once the tooth is fully formed and erupted, dental enamel has no regenerative capacity.

By weight, normal dental enamel is 96 percent mineral, 2 percent water, 1 percent protein, and 1 percent other components [2]. Mineralization occurs through the tightly controlled processing of the extracellular matrix and regulation of calcium and phosphate mineral deposition [3]. Fully developed enamel consists primarily of carbonate-substituted hydroxyapatite molecules that are organized into crystallites and arranged into interlocking prisms (picture 1). The structure of enamel provides its strength and resistance while making it less brittle.

Changes in the mineral, water, or protein content of enamel alter its appearance, strength, and resistance to wear and caries. As an example, substitution of fluorine for carbonate decreases the acid solubility of the enamel [4].

Dentin – Dentin is the most abundant dental tissue. It functions as the substructure for the enamel and largely determines the size and shape of teeth. Dentin is produced by odontoblast cells and the dental pulp. The production of dentin is increased in response to environmental stimuli such as trauma, tooth wear, or caries; reparative dentin is then deposited along the pulpal wall to protect the pulp from injury [5].

By weight, dentin contains approximately 60 percent mineral and 20 percent organic components, including protein. Type I collagen is the predominant dentin protein [6] and interacts with noncollagenous proteins to initiate and regulate mineralization [7].

Dentin is composed of a complex organization of tubules (picture 2) that are filled with fluid or the cellular processes of the odontoblasts and are thought to have a role in the neurosensory function of teeth [6]. The structure and composition of dentin impart teeth with the ability to flex and absorb tremendous functional loads without fracturing.

Pulp – The dental pulp is a specialized tissue made of odontoblasts, fibroblasts, blood vessels, nerves, and a complex extracellular matrix. It provides the neurosensory function and reparative potential of teeth [5,8].

The pulp continues to produce small amounts of dentin throughout the life of a tooth as part of normal pulp physiology [9]. Maintaining a healthy dental pulp until the root of the tooth is fully formed and has walls thick enough to sustain the forces transmitted from the crown during mastication is important. The prognosis for successful endodontic treatment and tooth retention is diminished if the pulp becomes nonvital and dentin production stops before complete root formation, although pulp tissue in young teeth with incomplete closure of the apex can be regenerated [10]. Thus, prompt and appropriate treatment of dental trauma and caries in children is critical to the sustenance of oral health.

Cementum – Cementum is made of type I and other collagens, noncollagenous proteins, and a mineralized matrix. It covers the root surface and helps to prevent the tooth from becoming fused to or resorbed by the adjacent alveolar bone. It is structurally similar to bone, with cementocytes lying in lacunae and interconnected by canaliculi. In addition, cementum provides the tissues by which the tooth is anchored to the periodontal ligament and the alveolar bone [11]. The cementum, periodontal ligament, and alveolar bone form a flexible sling that holds the tooth in place while allowing the physiologic movement necessary under the forces required for chewing. All three of these tissues have some capacity to regenerate, allowing traumatized teeth (eg, tooth avulsion) or pathologic conditions (eg, periodontal disease) to be treated successfully in many cases [12].

DENTAL DEVELOPMENT — Dental development proceeds from approximately the sixth week in utero through late adolescence. It involves the formation, eruption, and shedding of the 20 primary (deciduous or shedding) teeth, as well as the formation and eruption of the 32 permanent teeth. Throughout this prolonged span of development, the teeth are subject to both genetic and environmental influences. The developmental processes related to timing, location, morphology, structure, and composition of teeth primarily are genetically controlled and are regulated by thousands of genes [13,14].

The early embryonic requirements for dental development are differentiation of the oral ectoderm and migration of neural crest cells into the craniofacial region where the tooth buds will ultimately form. Dental development begins at approximately the sixth week in utero, when the oral ectoderm starts to proliferate at the future sites of primary teeth. As the oral ectoderm proliferates, it forms nests in the underlying mesenchyme and eventually contacts and interacts with the neural crest-derived ectomesenchymal cells, initiating the development of the tooth bud primordia [15].

These early events in tooth development are regulated by the oral epithelium and require the expression of numerous genes, including transcription and growth factors [13,16]. Teeth do not develop, for example, in transgenic mice that are missing the transcription factors MSX1 and MSX2 [13].

The interaction between the ectodermal cells and the underlying ectomesenchymal cells leads to differentiation of the highly specialized cells that produce the dental tissues and establish the tooth size and shape. The location and tooth type (eg, incisor, cuspid, premolar, molar) are thought to be genetically determined through the differential expression of transcription factors in the regions of the developing teeth [17]. The ameloblasts, or enamel-forming cells, are derived from the oral epithelium; the odontoblasts that form dentin and pulp are derived from the ectomesenchymal cells; the cementoblasts are derived from the mesenchyme. For an intact and viable tooth to develop, each of these cell types must differentiate, produce, and process the extracellular matrix and regulate mineralization of the extracellular matrix.

Each of these steps is under strict genetic control and represents a potential pathway for a hereditary defect of dental development. (See "Developmental defects of the teeth".)

TOOTH ERUPTION — The process by which teeth emerge from their developmental crypt into the oral cavity is known as tooth eruption. It involves both the teeth and the tissues through which the emerging teeth pass [18,19].

Primary teeth eruption — The eruption of teeth typically is bilaterally symmetric, with the left and right teeth appearing at similar times. The mandibular central incisors typically are the first primary teeth to erupt, usually between 6 and 10 months of age (figure 2) [20]. The maxillary central incisors erupt next, followed by the lateral incisors, first molars, canines, and second molars, in sequential order. In general, the primary dentition is fully erupted by 30 months of age. By convention in the United States, dentists identify the primary teeth by the letters A through T (figure 3). Different identification systems are used in other countries. Variability in the timing and sequence of tooth eruption is to be expected for both primary and permanent teeth. Sex and race/ethnicity affect the timing of tooth eruption; females tend to develop their teeth earlier than do males, and Black children earlier than White children [21,22].

Teething symptoms — It is normal for infants whose primary teeth are erupting to be cranky, chew on objects, and have excessive drooling. Caregivers frequently report that their infants who are teething have fever, diarrhea, or other systemic symptoms [23-27]. A systematic review and meta-analysis determined that gingival irritation (87 percent), caregiver-reported irritability (68 percent), and drooling (56 percent) are the most common symptoms associated with tooth eruption [28]. Although tooth eruption was associated with an increase in temperature, it was not associated with fever (ie, >38°C [100.4°F]) [28]. Severe signs and symptoms should be evaluated before they are attributed to teething [29]. This is supported by an observational study in which all but 2 of 50 children who were admitted to the hospital with an initial complaint of teething were diagnosed with a medical condition (including bacterial meningitis in one child) [30]. In addition, a systematic review of prospective cohort studies [25,27,31] found no symptoms, signs, or clusters of symptoms and signs specific enough to teething to reliably exclude other clinically important conditions (eg, infection) [32].

The management of teething symptoms is palliative (eg, chewing on a chilled [not frozen] teething ring or other teething device, systemic analgesia). To prevent choking, teething rings and other chewing devices should be one piece. To prevent promotion of dental caries, these devices should not be dipped in sugary substances. Teething necklaces, bracelets, or anklets that are made of beads should be avoided because of the risk of choking, strangulation, injury to the mouth, and infection [33,34].

We do not recommend over-the-counter (including homeopathic remedies) or prescription-strength topical analgesics (eg, lidocaine, benzocaine) for teething pain. The benefit of topical gels or teething tablets in managing teething pain has not been demonstrated, and they may be harmful [35,36]. Laboratory analysis of some homeopathic remedies found greater amounts of Atropa belladonna (deadly nightshade, an anticholinergic agent) than claimed on the label [37,38]. Symptoms of belladonna toxicity include seizures, difficulty breathing, lethargy, excessive sleepiness, muscle weakness, skin flushing, constipation, difficulty urinating, and agitation [39]. Viscous lidocaine has been associated with serious adverse reactions (including death) in young children being treated for mouth pain, including teething [40]. Methemoglobinemia has been reported in association with the use of oral benzocaine sprays; benzocaine-containing teething gels should not be used in teething infants or children younger than two years of age [36,41-43]. (See "Anticholinergic poisoning", section on 'Clinical features of overdose' and "Clinical use of topical anesthetics in children", section on 'Benzocaine'.)

Primary tooth exfoliation — Primary tooth exfoliation occurs as part of the process of permanent tooth eruption, which usually begins at approximately six years of age (figure 4). The permanent tooth, which develops apical to the primary tooth, helps stimulate resorption of the primary tooth root as it migrates through the alveolar bone toward the oral cavity. As the permanent tooth nears the mucosal surface, most of the root of the primary tooth has been resorbed; the primary tooth begins to loosen and eventually falls out. Primary teeth lacking a permanent successor typically undergo root resorption and ultimately exfoliate, indicating genetic programming for root resorption.

Early exfoliation — Premature exfoliation of primary teeth (before the age of four years) can be caused by local factors or systemic health problems, some of which are life threatening (table 1). A thorough medical evaluation and referral to a pediatric dentist are indicated in cases of premature primary tooth exfoliation so that optimal and appropriate treatment, if necessary or available, can be initiated promptly. (See "Developmental defects of the teeth".)

Delayed exfoliation — Over-retention of the primary tooth can occur if during permanent tooth eruption the primary tooth root does not adequately resorb. As a consequence, the permanent tooth will often emerge ectopically (out of its normal position). Ectopic eruption of permanent teeth frequently occurs in the anterior region of the mandible, where the permanent teeth come in on the tongue side of the primary teeth (picture 3). In most cases, the primary tooth will exfoliate within one year without treatment; however, extraction occasionally is required.

Permanent teeth eruption — Permanent teeth usually begin to erupt at six years of age (figure 4). They enter the oral cavity when approximately two-thirds of the root is formed. Once permanent teeth have penetrated the oral soft tissue, they erupt at a rapid rate, continuing to emerge until they make contact with teeth or tissue in the opposing arch. Over-eruption of a new tooth can occur if opposition is lacking because of missing or malaligned teeth. The central incisors and first molars are the first permanent teeth to erupt, followed sequentially by the lateral incisors, canines, first premolars, second premolars, second molars, and third molars. By convention in the United States, general dentists identify the permanent teeth by the numbers 1 through 32 (figure 5).

Delayed eruption — If tooth eruption is delayed ≥6 months beyond the normal range for a particular tooth (ie, if the mandibular central incisors have not erupted by 16 months) or if there is asymmetric tooth eruption of ≥6 months, evaluation for causes other than normal variation may be warranted. Delays in dental eruption can be familial (eg, primary failure of tooth eruption [MIM #125350], caused by mutations in the PTH1R gene [MIM *168468]) [44] or can occur with conditions such as Down syndrome [45], hypothyroidism, hypopituitarism, achondroplastic dwarfism, osteopetrosis, rickets, or chondroectodermal dysplasia. Delayed or abnormal tooth eruption is also associated with enamel-renal syndrome and cleidocranial dysplasia [46]. Associated clinical features help to narrow the diagnostic possibilities, and the evaluation is tailored accordingly. (See "Down syndrome: Clinical features and diagnosis", section on 'Diagnosis of Down syndrome' and "Clinical features and detection of congenital hypothyroidism", section on 'Diagnosis' and "Diagnostic testing for hypopituitarism" and "Overview of rickets in children", section on 'Evaluation'.)

Complete failure of tooth eruption can occur for a variety of reasons, the most common being a lack of space [47]. Complete failure of tooth eruption also is associated with a variety of conditions, syndromes, and genetic variation (eg, Albright hereditary osteodystrophy, ectodermal dysplasias, William syndrome, oto-palatal-digital syndrome, selective tooth agenesis) [48-50]. (See "Developmental defects of the teeth".)

Radiographic evaluation can be helpful in delineating the cause of abnormalities in tooth eruption. It may be warranted when there is clinical evidence that one or more teeth has failed to erupt six months after the normal range for eruption.

Accelerated eruption — Accelerated eruption of the primary and/or permanent teeth can occur in a variety of conditions, including preterm birth, various syndromes, and obesity [51-54]. Accelerated dental eruption of the mixed dentition can occur in children for a variety of reasons, including dental caries in the primary dentition [55] and diabetes mellitus [56,57]. Dental maturity is accelerated in patients with Turner syndrome, but the timing of clinical eruption is normal [58].

SUMMARY

Dental development – Dental development proceeds from approximately the sixth week in utero through late adolescence. It involves the formation, eruption, and shedding of the 20 primary teeth, and the formation and eruption of the 32 permanent teeth. (See 'Dental development' above.)

Primary tooth eruption – The eruption of teeth typically is bilaterally symmetric, with the left and right teeth appearing at similar times. The mandibular central incisors are the first primary teeth to erupt, usually between 6 and 10 months of age (figure 2). The primary dentition usually is fully erupted by 30 months of age. (See 'Primary teeth eruption' above.)

Symptoms of teething include fussiness, mouthing behaviors, and drooling. Caregivers frequently report systemic symptoms (fever, diarrhea) associated with teething. These symptoms are not specific enough to teething to reliably exclude other clinically important conditions (eg, infection). The management of teething symptoms is palliative. (See 'Teething symptoms' above.)

Primary tooth exfoliation – Primary tooth exfoliation occurs as part of the process of permanent tooth eruption, which usually begins at approximately six years of age (figure 4). Premature exfoliation of primary teeth can be caused by local factors or systemic health problems, some of which are life threatening (table 1). (See 'Primary tooth exfoliation' above.)

Permanent teeth eruption – Permanent teeth usually begin to erupt at six years of age (figure 4). (See 'Permanent teeth eruption' above.)

Delayed eruption – Children whose teeth erupt six months or later than normal or who have asymmetric eruption should be evaluated for abnormal dental eruption, congenitally missing teeth, and various systemic conditions. (See 'Delayed eruption' above.)

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