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Dental enamel hypoplasia

Deficiency in enamel thickness caused by physiological stress during the secratory phase of amelogenesis. Hypoplasia can appear as any form of deficiency or absence (pits, vertical and horizontal grooves, combination of defects) of the enamel and may be seen on the tooth crown surface. Enamel hypoplasia is a non-specific and sensitive indicator of physiological stress.

A) Ante mortem loss of the second mandibular molar and resorption of the alveolar bone, B) Resorption of the alveolar bone crest revealing the bifurcation of the first mandibular molar root, C) Porosity of the alveolar bone indicating periodontal disease, D) Combination of hypoplastic defects affecting the mandibular canine buccal surface. (Peqiin, Chalcolithic Period circa. 6500BP).
 

Combination of hypoplastic defects affecting the mandibular canine buccal surface and linear form of hypoplasia especially affecting the premolars. (Peqiin, Chalcolithic Period circa. 6500BP).

 

Linear form of hypoplasia affecting the canine and arrow pointing to calculus accumulation on the buccal surface of the lateral mandibular incisor. (Shiqmim, Chalcolithic Period circa. 6500BP).

It may occur under circumstances such as: systematic metabolic stress (nutritional deficiency, infection and allergy), localized trauma or hereditary anomalies. Since enamel does not remodel, the occurrence of enamel hypoplasia is indicative of physiological stress during infancy and/or childhood at the time when enamel was formed.

 

Periodontal disease

A group of diseases (gingivitis, periodontitis, gingival abscess, periodontal abscess) that affect the soft and hard tissues supporting and anchoring the tooth. The consumption of soft sticky foods promotes the accumulation of plaque which plays a crucial role in the progression of periodontal disease. Accumulation of plaque and its subsequent calcification (infra/supra gingival calculus) may lead to chronic or acute gingival inflammation possibly resulting in the destruction of the periodontal ligament at the attachment along the root surface; the resorption of the alveolar bone crest and finally, the loss of the tooth prior to death.

Ante mortem tooth loss

Severe ante mortem tooth loss and alveolar bone resorption throughout the mandibular arch (Peqiin, Chalcolithic Period circa. 6500BP).

The loss of the tooth prior to death as a result of periodontal disease, pulp chamber infection or direct trauma. The loss of the tooth leads to the resorption of the supporting alveolar bone.

Caries

Arrows pointing to carious lesions in the mandibular teeth. (Atlit Yam, PPNC Period circa. 7500BP).

A disease process involving the localized destruction of the tooth crown. The etiology of caries is complex and there is no universal agreement as to its exact cause. Nevertheless, the most widely accepted theory is called the Acidogenic Theory in which caries is believed to be caused by acid producing bacteria during the enzymatic breakdown of dietary carbohydrates. The initial effect of the acid produced in this process is the demineralization of the enamel and dentine and later the destruction of the organic portion of the affected area. If the pulp chamber is infected an abscess (see below) may form and the tooth may be lost prior to death. Since dietary carbohydrates, especially refined sugar, play a major role in the caries process, the prevalence of caries can be used to make inferences regarding diet.

 

Dental wear

A process involving the wearing down of the tooth surfaces by several mechanisms which are not exclusive to each other: A) friction of tooth on tooth , B) friction of tooth against foreign materials, C) eroding chemical processes other than those involving bacteria. Wear is not defined as pathological unless it causes pulp chamber exposure, leading to the infection of the pulp. Diet is a major modifying factor in the wearing down of the tooth surface, a tough and/or abrasive and/or chemically erosive diet will lead to faster wear while a refined non-abrasive, non-erosive diet will lead to slower wear rate.

A) Ante mortem loss of the second mandibular molar, B) Occlusal wear with cupping of the dentin. (Peqiin, Chalcolithic Period circa. 6500BP).

The analysis of dental wear allows researchers to make inferences regarding diet, food processing methods, and the non-alimentary use of teeth. Since wear is highly correlated with age it is used as a tool in the assessment of individual age at death in archaeological skeletal samples. Nevertheless, since wear varies between populations and even individuals, specific wear rate calibration is needed before making any such estimation.



Periapical abscess

An accumulation of pus in a bone cavity around the root of the tooth, resulting from the infection of the pulp chamber which may be caused by a carious lesion, trauma or severe wear. Eventually the tooth can be lost prior to death.

Abscesses in the mandibular molar region, note the destruction of the alveolar bone. (Peqiin, Chalcolithic Period circa. 6500BP).
Maxilla showing multiple lesions in the alveolar bone (C, A) and ante mortem tooth loss (B). (Wadi Makkukh, Chalcolithic Period circa. 6500BP).
 
A) Abscess along the mesial root of the first mandibular molar, B) Burning. Note the severe occlusal wear in the molar. (Wadi Makkukh, Chalcolithic Period circa. 6500BP).

 

 

 

Stages of teeth development


Initiation
The first stage is the development of the dental lamina as a distinct narrow band in the developing jaws. It is composed of cells from the oral cavity ectoderm and underlying mesenchyme. Mesenchyme and ectoderm are of separate embryonic origin: the mesenchyme is from the internal part of the early embryo and is the initial tissue forming the internal organs such as bone and muscle, the ectoderm is from the external part and gives rise to skin and epithelium. The process is initiated by reciprocal signals in both tissues. Localized swellings appear in the dental lamina that define the location of the future tooth bud, this swelling is the dental placode.

Morphogenesis

Morphogenesis is the process of shape formation. The dental placode develops into the dental bud, in a process called budding, which entails a fold of both ectoderm and mesenchyme. Budding processes are also found in the creation of other organs such as hair follicles, mammary glands and feathers. The bud folds once again, this time internally and in an opposite direction to the first fold. This marks the beginning of the cap stage. In the topmost part of the cap the enamel knot appears, this is a group of cells that govern consecutive morphogenesis. The bottom and eccentric sides of the cap are called the cervical loop since they mark the location of the cervical portion of the crown. Further folding lead to the next stage of development the early bell stage. In multi-cusped teeth a primary enamel knot appears on the first cusp to develop and secondary enamel knots appear on each of the other cusps. In the early bell stage, each of the cusps is folded separately at the future occlusal portion of the tooth and the cervical loop extends towards the cervical portion of the tooth.

Differentiation and Mineralization
At the late bell stage the embryonic tissues differentiate into tissues capable of creating mineralized matrices. The ectoderm cells differentiate into ameloblasts which secrete a matrix that mineralizes to enamel and the mesenchyme cells differentiate into odontoblasts which secrete a matrix that mineralizes to dentin. Enamel and dentin are secreted peripherally from the junction of the ectoderm and mesenchyme. Enamel is secreted on top of the cusps and on the sides of the crown. In the root of the tooth cementum replaces enamel.


 

 
 

 

   
 
     
     
     
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