Iōng-chiá:Albert/Draft

Chiàⁿ-pêng ē-kha (ùi tò-chhiú-pêng kàu chiàⁿ-chhiú-pêng) tē-3, tē-2, kap tē-1 tōa-āu-chan ê tiān-kong-phìⁿ, ē-sái khòaⁿ-kìⁿ bô-kâng kai-tōaⁿ ê chhùi-khí hoat-io̍k.

Chhùi-khí hoat-io̍k ùi phoe-thai sè-pau, seng-tióng kàu puh-khí ji̍p kháu-khiuⁿ, sī ho̍k-cha̍p ê kòe-têng. Sui-bóng chē-chē bu̍t-chióng (species) ū chhùi-khí, in chhùi-khí ê hoat-io̍k kah jîn-lūi bô-siáⁿ-mi̍h bô-siâng. Nā-beh-ū khong-kiān ê kháu-khiuⁿ khoân-kéng, tī thai-jî hoat-io̍k ê sek-tòng kai-tōaⁿ lāi-té, khí-iū-chit, khí-pún-chit, khí-kut-chit, kap khí-chiu cho·-chit tio̍h-ài khai-sí hoat-io̍k. Gín-á-khí tī seⁿ-kiáⁿ-tē lāi-té tē-6 chì tē-8 lé-pài khai-sí hêng-sêng, ah tōa-lâng-khí tī seⁿ-kiáⁿ-tē ê tē-20 lé-pái khai-sí hêng-sêng. Khah-su chhùi-khí bô tī chit-ê sî-chūn khai-sí hoat-io̍k, in tio̍h bē hoat-io̍k.

Chiok-chē gián-kiù chù-bo̍k tī ín-khí chhùi-khí hoat-io̍k ê koan-chiàn kòe-têng. Tī tē-1 branchial arch ê cho·-chit lāi-té ū chhùi-khí hoat-io̍k pit-su-iàu ê in-sò·, che sī hō·-lâng kóng-hòan chiap-siu ê koān-tiám.

Khài-iàu

Chhùi-khí ìⁿ-gê ê cho·-chit chhiat-phìⁿ.
A: khí-iū-chit khì-koan (enamel organ)
B: chhùi-khí ni-thâu (dental papilla)
C: chhùi-khí lī-pau(dental follicle)

Chhùi-khí ìⁿ-gê sī lō·-bóe hêng-sêng chhùi-khí ê chi̍t-tīn sè-pau. Chia-ê sè-pau sī ùi tē-it branchial arch ê gōa-phoe-chân (ectoderm) kap sîn-keng-chiah (neural crest) ê ectomesenchyme ián-thòaⁿ--lâi-ē. Chhùi-khí ìⁿ-gê ē hun-hòa chò 3-ê pō·-hūn: khí-iū-chit khì-koan (enamel organ), chhùi-khí ni-thâu (dental papilla), chhùi-khí lī-pau (dental follicle).

Khí-iū-chit khì-koan sī iû gōa-kháu ê khí-iū-chit siōng-phôe (outer enamel epithelium), lāi-té ê khí-iū-chit siōng-phôe (inner enamel epithelium), stellate reticulum, kap stratum intermedium lâi cho·-sêng. Chit-kóa sè-pau sī ameloblast ê khí-goân. Ameloblast chè-chō khí-iū-chit kap reduced enamel epithelium. Gōa-kháu ê khí-iū-chit siōng-phôe kap lāi-té ê khí-iū-chit siōng-phôe sio-kap ê só·-chāi kiò-chò cervical loop. Cervical loop hia ê sè-pau kè-sio̍k ǹg koh-khah chhim ê cho·-chit só·-chāi seng-tióng, chiâⁿ-chò Hertwig's epithelial root sheath, i koat-tēng soah-chhiú chhùi-khí khí-kha ê hêng-chōng.

Chhùi-khí ni-thâu hâm-iú ē hoat-tián chò [[odontoblast] ê sè-pau, i sī hêng-sêng khí-pún-chit ê sè-pau. Chhùi-khí ni-thâu kap lāi-té ê khí-iū-chit siōng-phôe chih-chiap ê só·-chāi ē-tit koat-tēng āu--lâi chhùi-khí khí-koan ê hêng-chōng. Chhùi-khí ni-thâu tiong-hng ê mesenchyme sè-pau sī kah chhùi-khí khí-chhóe ê hêng-sêng ū tī-tāi.

Chhùi-khí lī-pau ē piàn-chò 3-ê chiâⁿ tiōng-iàu ê mi̍h-kiāⁿ: cementoblast, osteoblast, kap fibroblast. Cementoblast sán-seng chhùi-khí khí-kha piáu-bīn ê khí-kut-chit. Osteoblast seⁿ-chhut khí-kha sì-pêng ê khí-chô-kut. Fibroblast hoat-io̍k chhut khí-chiu jūn-tòa, i liân-chiap khí-chô-kut kap khí-kut-chit, choâⁿ kā chhùi-khí kò·-tēng tī-leh khí-chô.

Jîn-lūi chhùi-khí hoat-io̍k ê sî-kan-pió

Ē-kha chit-kóa pió siá--ê sī jîn-lūi chhùi-khí hoat-io̍k ê sî-kan. Gín-á-khí thâu-khí-seng kài-hòa ê sî-kan sī ēng seⁿ-kiáⁿ-tē lāi-té ê lé-pāi sò·-bo̍k piáu-sī.

	Téng-kiuⁿ (maxillary) chhùi-khí
Gín-á-khí	Chiàⁿ -mn̂g-khí	Chhek -mn̂g-khí	Kak-khí	Tē-1 āu-chan	Tē-2 āu-chan
Thâu-khí-seng ê kài-hòa	14 lé-pài	16  lé-pài	17 lé-pài	15.5 lé-pài	19 lé-pài
Khí-koan oân-sêng	1.5 goe̍h	2.5 goe̍h	9 goe̍h	6 goe̍h	11 goe̍h
Khí-kha oân-sêng	1.5 tang	2 tang	3.25 tang	2.5 tang	3 tang
	Ē-kiuⁿ (mandibular) chhùi-khí
Thâu-khí-seng ê kài-hòa	14 lé-pài	16 lé-pài	17 lé-pài	15.5 lé-pài	18 lé-pài
Khí-koan oân-sêng	2.5 goe̍h	3 goe̍h	9 goe̍h	5.5 goe̍h	10 goe̍h
Khí-kha oân-sêng	1.5 tang	1.5 tang	3.25 tang	2.5 tang	3 tang

	Téng-kiuⁿ chhùi-khí
Tōa-lâng-khí	Chiàⁿ -mn̂g-khí	Chhek -mn̂g-khí	Kak-khí	Tē-1 sió-āu-chan	Tē-2 sió-āu-chan	Tē-1 tōa-āu-chan	Tē-2 tōa-āu-chan	Tē-3 tōa-āu-chan
Thâu0khí-seng ê kài-hòa	3–4 goe̍h	10–12 goe̍h	4–5 goe̍h	1.5–1.75 tang	2–2.25 tang	chhut-sì ê sî	2.5–3 tang	7–9 tang
Khí-koan oân-sêng	4–5 tang	4–5 tang	6–7 tang	5–6 tang	6–7 tang	2.5–3 tang	7–8 tang	12–16 tang
Khí-kah oân-sêng	10 tang	11 tang	13–15 tang	12–13 tang	12–14 tang	9–10 tang	14–16 tang	18–25 tang
	Ē-kiuⁿ chhùi-khí
Thâu-khí-seng ê kài-hòa	3–4 goe̍h	3–4 goe̍h	4–5 goe̍h	1.5–2 goe̍h	2.25–2.5 goe̍h	chhut-sì ê sî	2.5–3 tang	8–10 tang
Khí-koan oân-sêng	4–5 tang	4–5 tang	6–7 tang	5–6 tang	6–7 tang	2.5–3 tang	7–8 tang	12–16 tang
Khí-kha oân-sêng	9 tang	10 tang	12–14 tang	12–13 tang	13–14 tang	9–10 tang	14–15 tang	18–25 tang

Chhùi-khí ìⁿ-gê ê hoat-io̍k

Tī hián-bî-kiàⁿ ē-té ē-ái kòaⁿ-kìⁿ ê chhùi-khí chiâⁿ-hêng ê siāng-khí-seng 1-pō· sī vestibular lamina kap dental lamina ê khu-pia̍t. Dental lamina liân-kiat hoat-io̍k ê chhùi-khí-ìⁿ kap kháu-khiuⁿ ê siōng-phôe-chân, chit-ê liân-kiat î-chhî bē-té ê 1-toaⁿ sî-kan.

Chhùi-khí ê hoat-io̍k thong-siông hun-chò ē-kha kúi-ê kai-toāⁿ: ìⁿ-gê kî, bō-á kî, leng-liang kî, kap siāng-loh-bóe ê sêng-se̍k kî. Chhùi-khí hoat-io̍k ê hun-kî sī siūⁿ-beh chiong sio-liân-soah hoat-seng ê kái-piàn chò hun-lūi; m̄-koh táu-té bó· 1-khí hoat-io̍k tiong ê chhùi-khí sī ūi-tī tó-chi̍t-ê hun-kî, che khak-si̍t sī chiâⁿ khùn-lân ê khang-khòe. Tio̍h-sǹg-sī kāng 1-khí hoat-io̍k tiong ê chhùi-khí, in-ūi bô-kâng phìⁿ ê cho·-chit chhiat-phìⁿ ê koan-hē, sú-tit hun-kî ê koat-tēng pìⁿ-chiâⁿ kēng-ka khùn-lân, ē chhut-hiān bô-kâng hun-kî ê kiat-kó.

Ì-gê kî

Ì-gê kî ê te̍k-sek sī chhùi-khí ìⁿ-gê ê sè-pau pâi-lia̍t iáu-koh chiâⁿ hùn-loān. Chit-ê kai-toāⁿ ê khai-sí sī siōng-phôe sè-pau cheng-seng chìn-ji̍p khí-chô-kut ê ectomesenchyme ê sî-chūn. Chhùi-khí ìⁿ-gê pún-sin sī dental lamina boa̍t-toan ê 1-tīn sè-pau.

Bô-á kî

Bô-á kî chhùi-khí ê cho·-chit chhiat-phìⁿ.

Tī bô-á kî, chhùi-khí ìⁿ-gê ê sè-pau chiah khai-sí pâi-lia̍t. Chi̍t-kóa ectomesenchymal cell thêng-chí sán-seng extracellular substances, án-ne tì-sú in chi̍p-chi̍p chò-hóe, hông kiò-chò chhùi-khí ni-thâu. Tī chit-ê sî-chūn, chhùi-khí ni-thâu piⁿ-á ê sè-pau pâi-lia̍t chiâⁿ-chò bô-á ê hêng-chōng, kiò-chò khí-iū-chit khì-koan (ū-lâng kā kiò-chò khí-pún-chit khì-koan). Koh-ū lēng-gōa chi̍t-tīn ectomesenchymal cell sio-chio óa-kīn chò-hóe, pau-ûi tī khí-iū-chit khì-koan kap chhùi-khí ni-thâu ê gōa-ûi. Soah--loh-lâi, khí-iū-chit khì-koan ē sán-seng khí-iū-chit, chhùi-khí ni-thâu ē sán-seng khí-pún-chit kap khí-chhóe, ah chhùi-khí lī-pau ē sán-seng só·-ū chhùi-khí ê chi-chhî kò·-chō.

Tī leng-liang kî khah-chá ê sî-chūn chhùi-khí ê cho·-chit chhiat-phìⁿ.

Bell stage

Leng-liang kî hoat-seng cho·-chit hun-hòa kap hêng-thāi hun-hòa. Khí-iū-chit khì-koan tī chit-sî sī leng-liang-á hêng, i tāi-pō·-hūn ê sè-pau seⁿ tio̍h chhiūⁿ thiⁿ-chhiⁿ, só·-í kiò-chò stellate reticulum. Khí-iū-chit khì-koan sì-chiu ê sè-pau hun-khui chò 3-chân. Khí-iū-chit khì-koan gōa-khau ê cuboidal cell kìo-chò gōa-khau ê khí-iū-chit siōng-phôe. Khí-iū-chit kap chhùi-khí ni-thâu sio-chiap ê hit chân sè-pau kiò-chò lāi-té ê khí-iū-chit siōng-phôe. Lāi-té ê khí-iū-chit siōng-phôe kap stellate reticulum chi-kan hit-chân kiò-chò stratum intermedium. Gōa-khau ê kap lāi-té ê khí-iū-chit siōng-phôe sio-chiap ê só·-chāi hêng-sêng 1-ê îⁿ-kho·-á, kiò-chò cervical loop.

Other events occur during the bell stage. The dental lamina disintegrates, leaving the developing teeth completely separated from the epithelium of the oral cavity; the two will not join again until the final eruption of the tooth into the mouth.

Histologic slide of tooth in late bell stage. Note disintegration of dental lamina at top.

The crown of the tooth, which is influenced by the shape of the internal enamel epithelium, also takes shape during this stage. Throughout the mouth, all teeth undergo this same process; it is still uncertain why teeth form various crown shapes—for instance, incisors versus canines. There are two dominant hypotheses. The "field model" proposes there are components for each type of tooth shape found in the ectomesenchyme during tooth development. The components for particular types of teeth, such as incisors, are localized in one area and dissipate rapidly in different parts of the mouth. Thus, for example, the "incisor field" has factors that develop teeth into incisor shape, and this field is concentrated in the central incisor area, but decreases rapidly in the canine area. The other dominant hypothesis, the "clone model", proposes that the epithelium programs a group of ectomesenchymal cells to generate teeth of particular shapes. This group of cells, called a clone, coaxes the dental lamina into tooth development, causing a tooth bud to form. Growth of the dental lamina continues in an area called the "progress zone". Once the progress zone travels a certain distance from the first tooth bud, a second tooth bud will start to develop. These two models are not necessarily mutually exclusive, nor does widely accepted dental science consider them to be so: it is postulated that both models influence tooth development at different times.

Other structures that may appear in a developing tooth in this stage are enamel knots, enamel cords, and enamel niche.

Histologic slide of developing hard tissues. Ameloblasts are forming enamel, while odontoblasts are forming dentin.

Crown stage

Hard tissues, including enamel and dentin, develop during the next stage of tooth development. This stage is called the crown, or maturation, stage by some researchers. Important cellular changes occur at this time. In prior stages, all of the inner enamel epithelium cells were dividing to increase the overall size of the tooth bud, but rapid dividing, called mitosis, stops during the crown stage at the location where the cusps of the teeth form. The first mineralized hard tissues form at this location. At the same time, the inner enamel epithelial cells change in shape from cuboidal to columnar. The nuclei of these cells move closer to the stratum intermedium and away from the dental papilla.

Histologic slide of tooth. Note the tubular appearance of dentin.
A: enamel
B: dentin

The adjacent layer of cells in the dental papilla suddenly increases in size and differentiates into odontoblasts, which are the cells that form dentin. Researchers believe that the odontoblasts would not form if it were not for the changes occurring in the inner enamel epithelium. As the changes to the inner enamel epithelium and the formation of odontoblasts continue from the tips of the cusps, the odontoblasts secrete a substance, an organic matrix, into their immediate surrounding. The organic matrix contains the material needed for dentin formation. As odontoblasts deposit organic matrix, they migrate toward the center of the dental papilla. Thus, unlike enamel, dentin starts forming in the surface closest to the outside of the tooth and proceeds inward. Cytoplasmic extensions are left behind as the odontoblasts move inward. The unique, tubular microscopic appearance of dentin is a result of the formation of dentin around these extensions.

After dentin formation begins, the cells of the inner enamel epithelium secrete an organic matrix against the dentin. This matrix immediately mineralizes and becomes the tooth's enamel. Outside the dentin are ameloblasts, which are cells that continue the process of enamel formation; therefore, enamel formation moves outwards, adding new material to the outer surface of the developing tooth.

Hard tissue formation

Sections of tooth undergoing development.

Enamel

See main article at Amelogenesis

Enamel formation is called amelogenesis and occurs in the crown stage of tooth development. "Reciprocal induction" governs the relationship between the formation of dentin and enamel; dentin formation must always occur before enamel formation. Generally, enamel formation occurs in two stages: the secretory and maturation stages. Proteins and an organic matrix form a partially mineralized enamel in the secretory stage; the maturation stage completes enamel mineralization.

In the secretory stage, ameloblasts release enamel proteins that contribute to the enamel matrix, which is then partially mineralized by the enzyme alkaline phosphatase. The appearance of this mineralized tissue, which occurs usually around the third or fourth month of pregnancy, marks the first appearance of enamel in the body. Ameloblasts deposit enamel at the location of what become cusps of teeth alongside dentin. Enamel formation then continues outward, away from the center of the tooth.

In the maturation stage, the ameloblasts transport some of the substances used in enamel formation out of the enamel. Thus, the function of ameloblasts changes from enamel production, as occurs in the secretory stage, to transportation of substances. Most of the materials transported by ameloblasts in this stage are proteins used to complete mineralization. The important proteins involved are amelogenins, ameloblastins, enamelins, and tuftelins. By the end of this stage, the enamel has completed its mineralization.

Dentin

See main article at Dentinogenesis

Dentin formation, known as dentinogenesis, is the first identifiable feature in the crown stage of tooth development. The formation of dentin must always occur before the formation of enamel. The different stages of dentin formation result in different types of dentin: mantle dentin, primary dentin, secondary dentin, and tertiary dentin.

Odontoblasts, the dentin-forming cells, differentiate from cells of the dental papilla. They begin secreting an organic matrix around the area directly adjacent to the inner enamel epithelium, closest to the area of the future cusp of a tooth. The organic matrix contains collagen fibers with large diameters (0.1-0.2 μm in diameter). The odontoblasts begin to move toward the center of the tooth, forming an extension called the odontoblast process. Thus, dentin formation proceeds toward the inside of the tooth. The odontoblast process causes the secretion of hydroxyapatite crystals and mineralization of the matrix. This area of mineralization is known as mantle dentin and is a layer usually about 150 μm thick.

Whereas mantle dentin forms from the preexisting ground substance of the dental papilla, primary dentin forms through a different process. Odontoblasts increase in size, eliminating the availability of any extracellular resources to contribute to an organic matrix for mineralization. Additionally, the larger odontoblasts cause collagen to be secreted in smaller amounts, which results in more tightly arranged, heterogenous nucleation that is used for mineralization. Other materials (such as lipids, phosphoproteins, and phospholipids) are also secreted.

Secondary dentin is formed after root formation is finished and occurs at a much slower rate. It is not formed at a uniform rate along the tooth, but instead forms faster along sections closer to the crown of a tooth. This development continues throughout life and accounts for the smaller areas of pulp found in older individuals. Tertiary dentin, also known as reparative dentin, forms in reaction to stimuli, such as attrition or dental caries.

Cross-section of tooth at root. Note clear, acellular appearance of cementum.
A: dentin
B: cementum

Cementum

Cementum formation is called cementogenesis and occurs late in the development of teeth. Cementoblasts are the cells responsible for cementogenesis. Two types of cementum form: cellular and acellular.

Acellular cementum forms first. The cementoblasts differentiate from follicular cells, which can only reach the surface of the tooth's root once Hertwig's Epithelial Root Sheath (HERS) has begun to deteriorate. The cementoblasts secrete fine collagen fibrils along the root surface at right angles before migrating away from the tooth. As the cementoblasts move, more collagen is deposited to lengthen and thicken the bundles of fibers. Noncollagenous proteins, such as bone sialoprotein and osteocalcin, are also secreted. Acellular cementum contains a secreted matrix of proteins and fibers. As mineralization takes place, the cementoblasts move away from the cementum, and the fibers left along the surface eventually join the forming periodontal ligmaments.

Cellular cementum develops after most of the tooth formation is complete and after the tooth occludes (in contact) with a tooth in the opposite arch. This type of cementum forms around the fiber bundles of the periodontal ligaments. The cementoblasts forming cellular cementum become trapped in the cementum they produce.

The origin of the formative cementoblasts is believed to be different for cellular cementum and acellular cementum. One of the major current hypotheses is that cells producing cellular cementum migrate from the adjacent area of bone, while cells producing acellular cementum arise from the dental follicle. Nonetheless, it is known that cellular cementum is usually not found in teeth with one root. In premolars and molars, cellular cementum is found only in the part of the root closest to the apex and in interradicular areas between multiple roots.

Histologic slide of tooth erupting into the mouth.
A: tooth
B: gingiva
C: bone
D: periodontal ligaments

Formation of the periodontium

The periodontium, which is the supporting structure of a tooth, consists of the cementum, periodontal ligaments, gingiva, and alveolar bone. Cementum is the only one of these that is a part of a tooth. Alveolar bone surrounds the roots of teeth to provide support and creates what is commonly called a "socket". Periodontal ligaments connect the alveolar bone to the cementum, and the gingiva is the surrounding tissue visible in the mouth.

Periodontal ligaments

Cells from the dental follicle give rise to the periodontal ligaments (PDL). Specific events leading to the formation of the periodontal ligaments vary between deciduous (baby) and permanent teeth and among various species of animals. Nonetheless, formation of the periodontal ligaments begins with ligament fibroblasts from the dental follicle. These fibroblasts secrete collagen, which interacts with fibers on the surfaces of adjacent bone and cementum. This interaction leads to an attachment that develops as the tooth erupts into the mouth. The occlusion, which is the arrangement of teeth and how teeth in opposite arches come in contact with one another, continually affects the formation of periodontal ligaments. This perpetual creation of periodontal ligaments leads to the formation of groups of fibers in different orientations, such as horizontal and oblique fibers.

Alveolar bone

As root and cementum formation begin, bone is created in the adjacent area. Throughout the body, cells that form bone are called osteoblasts. In the case of alveolar bone, these osteoblast cells form from the dental follicle. Similar to the formation of primary cementum, collagen fibers are created on the surface nearest the tooth, and they remain there until attaching to periodontal ligaments.

Like any other bone in the human body, alveolar bone is modified throughout life. Osteoblasts create bone and osteoclasts destroy it, especially if force is placed on a tooth. As is the case when movement of teeth is attempted through orthodontics, an area of bone under compressive force from a tooth moving toward it has a high osteoclast level, resulting in bone resorption. An area of bone receiving tension from periodontal ligaments attached to a tooth moving away from it has a high number of osteoblasts, resulting in bone formation.

Gingiva

The connection between the gingiva and the tooth is called the dentogingival junction. This junction has three epithelial types: gingival, sulcular, and junctional epithelium. These three types form from a mass of epithelial cells known as the epithelial cuff between the tooth and the mouth.

Much about gingival formation is not fully understood, but it is known that hemidesmosomes form between the gingival epithelium and the tooth and are responsible for the primary epithelial attachment. Hemidesmosomes provide anchorage between cells through small filament-like structures provided by the remnants of ameloblasts. Once this occurs, junctional epithelium forms from reduced enamel epithelium, one of the products of the enamel organ, and divides rapidly. This results in the perpetually increasing size of the junctional epithelial layer and the isolation of the remenants of ameloblasts from any source of nutrition. As the ameloblasts degenerate, a gingival sulcus is created.

Nerve and vascular formation

Frequently, nerves and blood vessels run parallel to each other in the body, and the formation of both usually takes place simultaneously and in a similar fashion. However, this is not the case for nerves and blood vessels around the tooth, because of different rates of development.

Nerve formation

Nerve fibers start to near the tooth during the cap stage of tooth development and grow toward the dental follicle. Once there, the nerves develop around the tooth bud and enter the dental papilla when dentin formation has begun. Nerves never proliferate into the enamel organ.

Vascular formation

Blood vessels grow in the dental follicle and enter the dental papilla in the cap stage. Groups of blood vessels form at the entrance of the dental papilla. The number of blood vessels reaches a maximum at the beginning of the crown stage, and the dental papilla eventually forms in the pulp of a tooth. Throughout life, the amount of pulpal tissue in a tooth decreases, which means that the blood supply to the tooth decreases with age. The enamel organ is devoid of blood vessels because of its epithelial origin, and the mineralized tissues of enamel and dentin do not need nutrients from the blood.

Tooth eruption

Tooth eruption occurs when the teeth enter the mouth and become visible. Although researchers agree that tooth eruption is a complex process, there is little agreement on the identity of the mechanism that controls eruption. Some commonly held theories that have been disproven over time include: (1) the tooth is pushed upward into the mouth by the growth of the tooth's root, (2) the tooth is pushed upward by the growth of the bone around the tooth, (3) the tooth is pushed upward by vascular pressure, and (4) the tooth is pushed upward by the cushioned hammock. The cushioned hammock theory, first proposed by Harry Sicher, was taught widely from the 1930s to the 1950s. This theory postulated that a ligament below a tooth, which Sicher observed on under a microscope on a histologic slide, was responsible for eruption. Later, the "ligament" Sicher observed was determined to be merely an artifact created in the process of preparing the slide.

The most widely held current theory is that while several forces might be involved in eruption, the periodontal ligaments provide the main impetus for the process. Theorists hypothesize that the periodontal ligaments promote eruption through the shrinking and cross-linking of their collagen fibers and the contraction of their fibroblasts.

Although tooth eruption occurs at different times for different people, a general eruption timeline exists. Typically, humans have 20 primary (baby) teeth and 32 permanent teeth. Tooth eruption has three stages. The first, known as deciduous dentition stage, occurs when only primary teeth are visible. Once the first permanent tooth erupts into the mouth, the teeth are in the mixed (or transitional) dentition. After the last primary tooth falls out of the mouth—a process known as exfoliation—the teeth are in the permanent dentition.

Primary dentition starts on the arrival of the mandibular central incisors, usually at eight months, and lasts until the first permanent molars appear in the mouth, usually at six years. The primary teeth typically erupt in the following order: (1) central incisor, (2) lateral incisor, (3) first molar, (4) canine, and (5) second molar. As a general rule, four teeth erupt for every six months of life, mandibular teeth erupt before maxillary teeth, and teeth erupt sooner in females than males. During primary dentition, the tooth buds of permanent teeth develop below the primary teeth, close to the palate or tongue.

Mixed dentition starts when the first permanent molar appears in the mouth, usually at six years, and lasts until the last primary tooth is lost, usually at eleven or twelve years. Permanent teeth in the maxilla erupt in a different order from permanent teeth on the mandible. Maxillary teeth erupt in the following order: (1) first molar (2) central incisor, (3) lateral incisor, (4) first premolar, (5) second premolar, (6) canine, (7) second molar, and (8) third molar. Mandibular teeth erupt in the following order: (1) first molar (2) central incisor, (3) lateral incisor, (4) canine, (5) first premolar, (6) second premolar, (7) second molar, and (8) third molar. Since there are no premolars in the primary dentition, the primary molars are replaced by permanent premolars. If any primary teeth are lost before permanent teeth are ready to replace them, some posterior teeth may drift forward and cause space to be lost in the mouth. This may cause crowding and/or misplacement once the permanent teeth erupt, which is usually referred to as malocclusion. Orthodontics may be required in such circumstances for an individual to achieve a straight set of teeth.

The permanent dentition begins when the last primary tooth is lost, usually at 11 to 12 years, and lasts for the rest of a person's life or until all of the teeth are lost (edentulism). During this stage, third molars (also called "wisdom teeth") are frequently extracted because of decay, pain or impactions. The main reasons for tooth loss are decay or periodontal disease.

Eruptions times for primary and permanent teeth

	Primary teeth
	Central incisor	Lateral incisor	Canine	First premolar	Second premolar	First molar	Second molar	Third molar
Maxillary teeth	10 mo	11 mo	19 mo			16 mo	29 mo
Mandibular teeth	8 mo	13 mo	20 mo			16 mo	27 mo
	Permanent teeth
	Central incisor	Lateral incisor	Canine	First premolar	Second premolar	First molar	Second molar	Third molar
Maxillary teeth	7–8 yr	8–9 yr	11–12 yr	10–11 yr	10–12 yr	6–7 yr	12–13 yr	17–21 yr
Mandibular teeth	6–7 yr	7–8 yr	9–10 yr	10–12 yr	11–12 yr	6–7 yr	11–13  yr	7–21 yr

Nutrition and tooth development

As in other aspects of human growth and development, nutrition has an effect on the developing tooth. Essential nutrients for a healthy tooth include calcium, phosphorus, fluoride, and vitamins A, C, and D. Calcium and phosphorus are needed to properly form the hydroxyapatite crystals, and their levels in the blood are maintained by Vitamin D. Vitamin A is necessary for the formation of keratin, as Vitamin C is for collagen. Fluoride is incorporated into the hydroxyapatite crystal of a developing tooth and makes it more resistant to demineralization and subsequent decay.

Deficiencies of these nutrients can have a wide range of effects on tooth development. In situations where calcium, phosphorus, and vitamin D are deficient, the hard structures of a tooth may be less mineralized. A lack of vitamin A can cause a reduction in the amount of enamel formation. Fluoride deficency causes increased demineralization when the tooth is exposed to an acidic environment, and also delays remineralization. Furthermore, an excess of fluoride while a tooth is in development can lead to a condition known as fluorosis.

Abnormalities

There are a number of tooth abnormalities relating to development.

Anodontia is a complete lack of tooth development, and hypodontia is a lack of some tooth development. Anodontia is rare, most often occurring in a condition called hipohidrotic ectodermal dysplasia, while hypodontia is one of the most common developmental abnormalities, affecting 3.5–8.0% of the population (not including third molars). The absence of third molars is very common, occurring in 20–23% of the population, followed in prevalence by the second premolar and lateral incisor. Hypodontia is often associated with the absence of a dental lamina, which is vulnerable to environmental forces, such as infection and chemotherapy medications, and is also associated with many syndromes, such as Down syndrome and Crouzon syndrome.

Hyperdontia is the development of extraneous teeth. It occurs in 1–3% of Caucasians and is more frequent in Asians. About 86% of these cases involve a single extra tooth in the mouth, most commonly found in the maxilla, where the incisors are located. Hyperdontia is believed to be associated with an excess of dental lamina.

Dilaceration is an abnormal bend found on a tooth, and is nearly always associated with trauma that moves the developing tooth bud. As a tooth is forming, a force can move the tooth from its original position, leaving the rest of the tooth to form at an abnormal angle. Cysts or tumors adjacent to a tooth bud are forces known to cause dilaceration, as are primary (baby) teeth pushed upward by trauma into the gingiva where it moves the tooth bud of the permanent tooth.

Regional odontodysplasia is rare, but is most likely to occur in the maxilla and anterior teeth. The cause is unknown; a number of causes have been postulated, including a disturbance in the neural crest cells, infection, radiation therapy, and a decrease in vascular supply (the most widely held hypothesis). Teeth affected by regional odontodysplasia never erupt into the mouth, have small crowns, are yellow-brown, and have irregular shapes. The appearance of these teeth in radiographs is translucent and "wispy," resulting in the nickname "ghost teeth".

Tooth development in animals

Generally, tooth development in non-human mammals is similar to human tooth development. The variations lie in the morphology, number, development timeline, and types of teeth, not usually in the actual development of the teeth.

Enamel formation in non-human mammals is almost identical to that in humans. The ameloblasts and enamel organ, including the dental papilla, function similarly. Nonetheless, while ameloblasts die in humans and most other animals—making further enamel formation impossible—rodents continually produce enamel, forcing them to wear down their teeth by gnawing on various materials. If rodents are prevented from gnawing, their teeth eventually puncture the roofs of their mouths. In addition, rodent incisors consist of two halves, known as the crown and root analogues. The labial half is covered with enamel and resembles a crown, while the lingual half is covered with dentin and resembles a root. Both root and crown develop simultaneously in the rodent incisor and continue to grow for the life of the rodent.

Unlike most animals, sharks continuously produce new teeth throughout life via a drastically different mechanism. Because shark teeth have no roots, sharks easily lose teeth when they feed (zoologists estimate that a single shark can lose up to 2,400 teeth in one year ), and must therefore be continually replaced. Shark teeth form from modified scales near the tongue and move outward on the jaw in rows until they fully develop, are used, and are eventually dislodged.

The mineral distribution in rodent enamel is different from that of monkeys, dogs, pigs, and humans. In horse teeth, the enamel and dentin layers are intertwined, which increases the strength and decreases the wear rate of the teeth.

Supporting structures that create a "socket" are found exclusively in mammals and Crocodylia. In manatees, mandibular molars develop separately from the jaw, and are encased in a bony shell separated by soft tissue. This also occurs in elephants' successional teeth, which erupt to replace lost teeth.

Notes

1. ^ A. R. Ten Cate, Oral Histology: Development, Structure, and Function, 5th ed. (Saint Louis: Mosby-Year Book, 1998), p. 95.
2. ^ Cate, Oral Histology, p. 81.
3. ^ University of Texas Medical Branch.
4. ^ Cate, Oral Histology, p. 102.
5. ^ University of Texas Medical Branch.
6. ^ Cate, Oral Histology, p. 86.
7. ^ University of Texas Medical Branch.
8. ^ Cate, Oral Histology, p. 86 and 102.
9. ^ Ross, Michael H., Gordon I. Kaye, and Wojciech Pawlina. "Histology: a text and atlas." 4th ed, p. 453.
10. ^ Ash & Nelson, Wheeler's Dental Anatomy, Physiology, and Occlusion, pp. 32, 45, and 53.
11. ^ University of Southern California School of Dentistry, The Bell Stage: Image 26 found here.
12. ^ Cate, Oral Histology, p. 81.
13. ^ Cate, Oral Histology, p. 82.
14. ^ Cate, Oral Histology, p. 84.
15. ^ Cate, Oral Histology, p. 84.
16. ^ University of Texas Medical Branch.
17. ^ University of Southern California School of Dentistry, The Bell Stage: Image 30 found here.
18. ^ Cate, Oral Histology, p. 87.
19. ^ Cate, Oral Histology, p. 89.
20. ^ Cate, Oral Histology, p. 86.
21. ^ Cate, Oral Histology, p. 95.
22. ^ Ross, Kaye, and Pawlina, Histologoy: a text and atlas, p. 444.
23. ^ Cate, Oral Histology, p. 95.
24. ^ Cate, Oral Histology, p. 197.
25. ^ Ross, Kaye, and Pawlina, Histology: Text and Atlas, p. 445.
26. ^ Ross, Kaye, and Pawlina, Histology: Text and Atlas, p. 447.
27. ^ Cate, Oral Histology, p. 136.
28. ^ Cate, Oral Histology, p. 95.
29. ^ Cate, Oral Histology, p. 138.
30. ^ Cate, Oral Histology, p. 139.
31. ^ Summitt, Fundamentals of Operative Dentistry, p. 13.
32. ^ Cate, Oral Histology, p. 128.
33. ^ Summitt, Fundamentals of Operative Dentistry, p. 183.
34. ^ Johnson, Biology of the Human Dentition, p. 183.
35. ^ Cate, Oral Histology, p. 236.
36. ^ Cate, Oral Histology, p. 241.
37. ^ Cate, Oral Histology, pp. 241 and 243.
38. ^ Cate, Oral Histology, p. 241.
39. ^ Cate, Oral Histology, p. 245.
40. ^ Ross, Kaye, and Pawlina, Histology: Text and Atlas, p. 453.
41. ^ Cate, Oral Histology, p. 245.
42. ^ Cate, Oral Histology, p. 244.
43. ^ Ross, Kaye, and Pawlina, Histology: Text and Atlas, p. 452.
44. ^ Cate, Oral Histology, pp. 247 and 248.
45. ^ Cate, Oral Histology, p. 248.
46. ^ Cate, Oral Histology, p. 93.
47. ^ Cate, Oral Histology, p. 93.
48. ^ Cate, Oral Histology, p. 93.
49. ^ Ross, Kaye, and Pawlina, Histology: Text and Atlas, p. 452.
50. ^ Riolo and Avery, Essentials for Orthodontic Practice, p. 142.
51. ^ Harris, Craniofacial Growth and Devleopment, pp. 1-3.
52. ^ Harris, Craniofacial Growth and Devleopment, p. 3.
53. ^ Harris, Craniofacial Growth and Devleopment, p. 5.
54. ^ The American Dental Association, Tooth Eruption Charts found here.
55. ^ Ash & Nelson, Wheeler's Dental Anatomy, Physiology, and Occlusion, pp. 38 and 41.
56. ^ Ash & Nelson, Wheeler's Dental Anatomy, Physiology, and Occlusion, pp. 38.
57. ^ WebMd, Dental Health: Your Child's Teeth found here.
58. ^ Ash & Nelson, Wheeler's Dental Anatomy, Physiology, and Occlusion, pp. 41.
59. ^ Monthly Microscopy Explorations, Exploration of the Month: January 1998 found here.
60. ^ Health Hawaii, Primary Teeth: Importance and Care found here.
61. ^ American Academy of Periodontology, Oral Health Information for the Public found here.
62. ^ Ash & Nelson, Wheeler's Dental Anatomy, Physiology, and Occlusion, p. 53.
63. ^ The American Dental Hygiene Association, Nutritional Factors in Tooth Development found here.
64. ^ Ross, Kaye, and Pawlina, Histology: Text and Atlas, p. 453.
65. ^ The American Dental Hygiene Association, Table II. Effects of nutrient deficiencies on tooth development found here.
66. ^ Neville, Damm, Allen, and Bouquot, Oral & Maxillofacial Pathology, p. 70.
67. ^ Neville, Damm, Allen, and Bouquot, Oral & Maxillofacial Pathology, p. 70.
68. ^ Kahn, Basic Oral & Maxillofacial Pathology, p. 49.
69. ^ Neville, Damm, Allen, and Bouquot, Oral & Maxillofacial Pathology, p. 86.
70. ^ Neville, Damm, Allen, and Bouquot, Oral & Maxillofacial Pathology, p. 99.
71. ^ Kahn, Basic Oral & Maxillofacial Pathology, p. 58.
72. ^ Frandson and Spurgeon, Anatomy and Physiology of Farm Animals., p. 305.
73. ^ Caceci. Veterinary Histology with subtitle "Digestive System: Oral Cavity" found here.
74. ^ Dave Abbott, Sharks, found here.
75. ^ Jason Buchheim, A Quick Course in Ichthyology, found here.
76. ^ Michael E. Williams, Jaws: The early years, found here.
77. ^ Fejerskov, O. on Pubmed. Link can be found here
78. ^ Randall-Bowman, whose article can be found here, and Encarta, whose link can be found here
79. ^ Cate, Oral Histology, p. 236.

References

• Abbott, Dave. "Sharks". 2000. Page accessed January 7, 2006.
• The American Academy of Periodontology. "Oral Health Information for the Public". Retrieved December 12, 2005.
• The American Dental Association. "Tooth Eruption Charts". Retrieved December 12, 2005.
• The American Dental Hygiene Association. "Nutritional Factors in Tooth Development". Retrieved December 10, 2005.
• The American Dental Hygiene Association. "Table II. Effects of nutrient deficiencies on tooth development". Retrieved December 10, 2005.
• Ash, Major M. and Stanley J. Nelson. Wheeler’s Dental Anatomy, Physiology, and Occlusion. 8th edition. 2003. ISBN 0721693822.
• Buchheim, Jason. "A Quick Course in Ichthyology". Page accessed January 7, 2006.
• Cate, A.R. Ten. Oral Histology: development, structure, and function. 5th ed. 1998. ISBN 0815129521.
• Caceci, Thomas. Veterinary Histology with subtitle "Digestive System: Oral Cavity". Retrieved December 15, 2005.
• Frandson, R.D. & T.L. Spurgeon, 1992. Anatomy and Physiology of Farm Animals. 5th edition. Philadelphia, Lea & Febiger. ISBN 0812114353.
• Harris, Edward F. Craniofacial Growth and Development. In the section entitled "Tooth Eruption." 2002.
• Health Hawaii. "Primary Teeth: Importance and Care". Retrieved December 12, 2005.
• Johnson, Clarke. "Biology of the Human Dentition". 1998.
• Kahn, Michael A. Basic Oral and Maxillofacial Pathology. Volume 1. 2001.
• Monthly Microscopy Explorations. "Exploration of the Month: January 1998". Retrieved December 12, 2005.
• Neville, B.W., Douglas Damm, Carl Allen, Jerry Bouquot. Oral & Maxillofacial Pathology. 2nd edition. 2002. ISBN 0721690033.
• Randall-Bowman, 2004. "Gummed Out: Young Horses Lose Many Teeth, Vet Says." April 2004. Article found here. Retrieved January 7, 2006.
• Riolo, Michael L. and James K. Avery. Essentials for Orthodontic Practice. 1st edition. 2003. ISBN 097205460X.
• Ross, Michael H., Gordon I. Kaye, and Wojciech Pawlina. Histology: a text and atlas. 4th edition. 2003. ISBN 0683302426.
• Summit, James B., J. William Robbins, and Richard S. Schwartz. Fundamentals of Operative Dentistry: A Contemporary Approach. 2nd edition. Carol Stream, Illinois, Quintessence Publishing Co, Inc. 2001. ISBN 0867153822.
• University of Southern California School of Dentistry. "The Bell Stage: Image 26". Retrieved December 11, 2005.
• University of Southern California School of Dentistry. "The Bell Stage: Image 30". Retrieved December 11, 2005.
• University of Texas Medical Branch. "Lab Exercises: Tooth development." Page found here.
• Williams, Michael E. "Jaws: The early years". 1992. Page accessed January 7, 2006.
• WebMd. "Dental Health: Your Child's Teeth". Retrieved December 12, 2005.

External links

• Bio-anthropology and ancient DNA
• Database on the expression of different genes in the developing tooth.
• Integumentary Development Tooth by Dr. Mark Hill from the University of New South Wales Embryology Resource
• Veterinary Histology by Dr. Thomas Caceci.