Tooth enamel

From Biocrawler, the free encyclopedia.

Tooth enamel is the most highly mineralized and hardest substance of the body ^{[1] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_body)}. Among enamel, dentin, and cementum, enamel is the dental tissue of a tooth which usually is visible in the mouth and must be supported by underlying dentin. Minerals compose 96% of enamel, with the rest being water and organic material ^{[2] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_organic)}. Since enamel is semi-translucent, the color of dentin and any restorative dental material underneath the enamel highly affects the outer appearance of the tooth. The color of enamel is a light yellow to grayish white. It varies in thickness over the surface of the tooth. Often, the cusp is the location where the enamel is thickest, up to 2.5 mm, and the thickness tapers down to a miniscule amount at its border, which is clinically seen as the cementoenamel junction (CEJ)^{[3] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_thickness)}.

The primary mineral component is hydroxyapatite, which is a crystalline calcium phosphate ^{[4] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_biology_hydroxy)}. This very large amount of minerals accounts for the strength of enamel, but also for its brittleness ^{[5] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_brittle)}. Thus, dentin, which is less mineralized and less brittle, compensates for enamel and is necessary as a support ^{[6] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_biology_dentin)}.

The organic portion of enamel does not contain collagen, as dentin and bone does. Instead, it has two unique classes of proteins called amelogenins and enamelins. The role of these proteins is not understood fully at this time, but it is believed that these proteins aid in the development of enamel as a framework support and other mechanisms ^{[7] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_framework)}.

Contents

1 Structure 2 Development 3 Destruction 4 Oral hygiene and fluoride 5 Effects of Dental Procedures on Enamel 5.1 Dental Restorations 5.2 Acid-Etching Techniques 5.3 Tooth Whitening 6 Other anatomical features of enamel 7 Enamel Disorders 8 Enamel in non-human Animals 9 See also 10 References 11 Notes

Structure

The basic unit of enamel is called an enamel rod ^{[8] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_biology_enamelrod)}. Measuring 4 μm wide to 8 μm high, an enamel rod (the antiquated term being enamel prism) is a tightly packed mass of hydroxyapatite crystals in an organized pattern ^{[9] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_pattern)}. In cross section, it is best compared to a keyhole with the top, or head, oriented toward the crown of the tooth and the bottom, or tail, oriented toward the root of the tooth.

It should be noted that the arrangement of the crystals within each enamel rod is highly complex and is not fully explained here. Both the cells, which initiated enamel formation, known as ameloblasts, and Tomes’ processes affect the crystals’ pattern. Basically, the enamel crystals are oriented parallel to the long axis of the rod when the crystal is in the head of the enamel rod ^{[10] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cateross_parallel)}. When found in the tail of the enamel rod, the crystal’s orientation diverges slightly from long axis ^{[11] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_diverges)}.

The arrangement of enamel rods is understood more clearly. Enamel rods are found in rows along the tooth. Within each row, the long axis of the enamel rod generally is perpendicular to the underlying dentin ^{[12] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_perpendicular)}. In permanent teeth, the enamel rods near the cementoenamel junction (CEJ) tilt slightly more toward the root of the tooth than would be expected. Knowing the orientation of enamel is very important in restorative dentistry because enamel unsupported by underlying dentin is prone to fracture and usually is avoided ^{[13] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_fracture)}.

The area around the enamel rod is known as interrod enamel. Interrod enamel has the same composition as the enamel rods. Nonetheless, a histologic distinction is made between the two because crystal orientation is different in each ^{[14] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_distinction)}.

Development

Enamel formation takes place in an overall process of tooth development. When the tissues of the developing tooth are seen under a microscope, different cellular aggregations can be identified, including structures known as the enamel organ, dental lamina, and dental papilla ^{[15] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_enamelorgan)}. The stages of tooth development generally recognized are the bud stage, cap stage, bell stage, and crown (or calcification) stage. Enamel formation is first seen under the microscope in the crown stage.

Amelogenesis, or enamel formation, occurs after the first establishment of dentin and via cells known as ameloblasts. Human enamel forms at a rate of ~4 μm per day and begins at the future location of cusps around 3-4 months in utero ^{[16] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_formationrate)}. As in all human processes, the creation of enamel is complex, but it would be fitting to view the process in two stages ^{[17] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_stages)}. The first stage, called the secretory stage, involves proteins and the organic matrix and results in a partially mineralized enamel. The second stage, called the maturation stage, completes enamel mineralization.

In the secretory stage, the ameloblasts are polarized columnar cells. In the rough endoplasmic reticulum of these cells, enamel proteins are released into the surrounding area and contributes to what is known as the enamel matrix, which almost immediately mineralizes partially by the enzyme, alkaline phosphatase ^{[18] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_phosphatase)}. When this first layer is formed, the ameloblasts move away from the dentin, allowing for the development of Tomes’ processes at the apical pole of the cell. Enamel formation continues around the adjoining ameloblasts, resulting in a walled area resembling a pit into which the Tomes’ process lies, and around the end of the Tomes’ process, resulting in deposition of matrix inside the pits ^{[19] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_pits)}. The matrix within the pits will eventually become enamel rods, and the walls will eventually become interrod enamel. The only distinguishing factor between the two is the orientation of the crystals.

In the maturation stage, the ameloblasts act as cells transporting substances for the formation of enamel. Histologically, the most notable aspect of this phase is that these cells become striated or have a ruffled border ^{[20] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_ruffled)}. These signs demonstrate that the ameloblasts have changed their function from production as in the secretory stage to transportation. Proteins compose most of the transported material. These are used for the final mineralization process. The noteworthy proteins involved are amelogenins, ameloblastins, enamelins, and tuftelins ^{[21] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_proteins)}. During this process, amelogenins and ameloblastins are removed after use, leaving enamelins and tuftelin in the enamel ^{[22] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_proteins2)}. By the end of this stage, the enamel has completed its mineralization.

Sometime before the tooth erupts into the mouth, but after the maturation stage, the ameloblasts are broken down. Consequently, enamel has no way of regenerating itself as many other tissues of the body ^{[23] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_regenerating)}. After destruction of enamel from decay or injury, neither the body nor a dentist can restore the enamel tissue. Enamel can be affected further from non-pathologic processes. The discoloration of teeth over time can result from exposure to substances such as tobacco, coffee, and tea ^{[24] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_adha_staining)}. This is partly due to material building up in the enamel, but is also an effect from the underlying dentin becoming sclerotic ^{[25] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summit_scleroticdentin)}. As a result, tooth color gradually darkens with age. Additionally, enamel becomes less permeable to fluids, less soluable to acid, and less composed of water ^{[26] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summit_enamelless)}.

Progress of Enamel Formation for Primary Teeth ^{[27] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_wheeler_enamelformationchart)}

		Amount of Enamel Formed at Birth	Enamel Mineralization Completed
Primary Maxillary Tooth	Central Incisor	5/6	1.5 months after birth
	Lateral Incisor	2/3	2.5 months after birth
	Canine	1/3	9 months after birth
	1st Molar	Cusps united; occlusal completely calcified and 1/2 to 3/4 crown height	6 months after birth
	2nd Molar	Cusps united; occlusal incompletely calcified; calcified tissue covers 1/5 to 1⁄4 crown height	11 months after birth
Primary Mandibular Tooth	Central Incisor	3/5	2.5 months after birth
	Lateral Incisor	3/5	3 months after birth
	Canine	1/3	9 months after birth
	1st Molar	cusps united; occlusal completely calcified	5.5 months after birth
	2nd Molar	cusps united; occlusal incompletely calcified	10 months after birth

Destruction

The high mineral content of enamel, which makes this tissue the hardest in the human body, also makes it susceptible to a demineralization process which often occurs as dental caries, otherwise known as cavities ^{[28] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_caries)}. There are many reasons for demineralization to occur. The most important cause of tooth decay is the ingestion of sugars.

Sugars from candies, soft drinks, and even fruit juices play a significant role in tooth decay, and consequently in enamel destruction. There is already a great number and variety of bacteria residing in the mouth. When sucrose, the most common of sugars, coats the surface of the mouth, some intraoral bacteria interact with it and form lactic acid ^{[29] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_lacticacid)}. Acid decreases the pH in the mouth. Then, the hydroxyapatite crystals of enamel demineralize, allowing for greater bacterial invasion further into the tooth. The most important bacteria involved with tooth decay is Streptococcus mutans, but the number and type of bacteria varies with the progress of tooth destruction ^{[30] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_streptmutans)}.

Furthermore, tooth morphology dictates the most likely locations for decay to occur. The most common site for the initiation of dental caries is in the deep grooves, pits, and fissures of enamel. This is expected because these locations are impossible to reach with a toothbrush and allow for bacteria to reside. When demineralization of enamel occurs, a dentist can use a sharp instrument, such as a dental explorer, and “feel a stick” at the location of the decay. As enamel continues to become less mineralized and is unable to prevent the encroachment of bacteria, the underlying dentin becomes affected as well. When dentin, which normally supports enamel, is destroyed by a physiologic condition or by decay, enamel is unable to compensate for its brittleness and breaks away from the tooth easily.

The extent to which tooth decay is likely, known as cariogenicity, depends upon factors such as how retentive the sugar is to the teeth. Unlike what is commonly believed, it is not the amount of sugar ingested but the frequency of sugar ingestion that is the most important factor in the causation of tooth decay. When the pH in the mouth initially decreases from the ingestion of sugars, the enamel is demineralized and left vulnerable for about 30 minutes. Eating a greater quantity of sugar in one sitting does not increase the time of demineralization. Similarly, eating a lesser quantity of sugar in one sitting does not decrease the time of demineralization. Thus, a great quantity of sugar at one time in the day will be less detrimental than a very small quantity ingested in many intervals throughout the day. For example, in terms of oral health, it is better to eat a very large dessert at dinnertime than to snack on a single, small bag of candy throughout the entire workday.

In addition to bacterial invasion, enamel is susceptible to other means of destruction as well. Bruxism, also known as clenching of or grinding on teeth, destroys enamel very quickly. The wear rate of enamel, called attrition, is 8 micrometers a year from normal factors. A common misperception is that enamel wears away mostly from chewing, but actually teeth rarely touch during chewing. Furthermore, normal tooth contact is compensated physiologically by the periodontal ligaments (pdl) and the arrangement of dental occlusion. The truly destructive forces are the parafunctional movements, as found in bruxism, and can cause irreversible damage to the enamel.

Other non-bacterial processes of enamel destruction include abrasion (involving foreign elements, such as a toothbrushes), erosion (involving chemical processes, such as lemon juice), and possibly abfraction (involving compressive and tensile forces) ^{[31] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_jcdp_toothwear)}.

Oral hygiene and fluoride

Considering the vulnerability of enamel to demineralize and the daily menace of sugar ingestion, prevention of tooth decay is the best way to maintain the health of teeth. Most countries have wide use of toothbrushes, whose purpose is to reduce the number of bacteria and food particles particularly on enamel. Some isolated societies in the world do not have access to toothbrushes, but it is common for those people to use other objects, such as sticks, to clean their teeth. In between two adjacent teeth, floss is used wipe the enamel surfaces free of plaque and food particles to discourage bacterial growth. Although neither floss nor toothbrushes can penetrate the deep grooves and pits of enamel, general oral health can usually prevent enough bacterial growth to keep tooth decay from starting.

These methods of oral hygiene have been helped greatly with the use of fluoride. Fluoride can be found in many locations naturally. It can be found in a variety water sources, the ocean being a notable example. Consequently, many seafood dishes contain fluoride as well. The recommended dosage of fluoride in drinking water is 1 part per million (ppm) ^{[32] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_dean_onepart)}. Fluoride helps prevent dental decay by binding to the hydroxyapatite crystals in enamel ^{[33] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_binding)}. The incorporated fluoride makes enamel more resistant to demineralization and, thus, resistant to decay ^{[34] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ross_resistant)}. Fluoride therapy is used to help teeth prevent dental decay.

Many groups of people have spoken out against fluorinated drinking water. One example used by these advocates is the damage fluoride can do as fluorosis. Fluorosis is a condition resulting from the overexposure to fluoride, especially between the ages of 6 months to 5 years, and appears as mottled enamel ^{[35] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_mottled)}. Consequently, the teeth look unsightly and, indeed, the incidence of dental decay in those teeth is very small. In spite of this, most substances, even helpful ones, taken in extreme are detrimental. Where fluoride is found naturally in high concentrations, filters are often used to decrease the amount of fluoride in water. For this reason, codes have been developed by dental professionals to limit the amount of fluoride a person should take ^{[36] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ada_fluoridecode)}. These codes are supported by the American Dental Association and the American Academy of Pediatric Dentistry. The acute toxic dose of fluoride is ~5 mg/kg of body weight. Furthermore, whereas topical fluoride, found in toothpaste and mouthwashes, does not cause fluorosis, its effects are also less pervasive and not as long-lasting as those of systemic fluoride, such as when drinking fluorinated water ^{[37] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_newbrun_systemic)}. For instance, all of a tooth's enamel gains the benefits of fluoride when it is ingested systemically, through fluorinate water or salt fluoridation (a common alternative in Europe). Only some of the outer surfaces of enamel can be reached by topical fluoride. Thus, one of the greatest successes in dental health care has been the inclusion of fluoride in public water to decrease tooth decay.

Effects of Dental Procedures on Enamel

Dental Restorations

Most dental restorations involve the removal of enamel. Frequently, the main purpose for its removal is to gain access to the underlying decay in the dentin or inflammation in the pulp. This is typically the case for amalgam restorations and endodontic treatment.

Nonetheless, enamel can sometimes be removed before there is any decay present. The process of placing dental sealants involves removing healthy enamel in the deep fissures and grooves of a tooth and replacing it with a restorative material ^{[38] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summitt_sealantprevention)}. Sealants are unique in that they are preventative restorations for protection from future decay and have shown to reduce the risk of decay by 55% over 7 years ^{[39] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summitt_reducerisk)}.

Additionally, esthetics can be another reason for the removal of enamel. This is a necessary practice when placing crowns and veneers to enhance the appearance of teeth. In both of these instances, it is important to keep in mind the orientation of enamel rods because it is possible to leave enamel unsupported by underlying dentin, leaving that portion of the prepared teeth more vulnerable to fracture ^{[40] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summitt_unsuportedenamel)}.

Acid-Etching Techniques

Invented in 1955, acid-etching employs the use of dental etchants and is used frequently when bonding dental restoration to teeth ^{[41] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summitt_acidetching)}. This is important for long-term use of some materials, such as composites and sealants ^{[42] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_materials)}. Acting by dissolving minerals in enamel, etchants remove the outer 10 micrometers on the enamel surface and makes a porous layer 5 - 50 micrometers deep ^{[43] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summitt_porouslayer)}. This roughens the enamel microscopically and results in a greater surface area on which to bond.

The effects of acid-etching on enamel can vary. Important variables are the amount of time the etchant is applied, the type of etchant used, and the current condition of the enamel ^{[44] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summitt_variables)}.

There are three types of pattern found from acid-etching ^{[45] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summitt_patterns)}. Type 1 is a pattern where predominantly the enamel rods are dissolved; type 2 is a pattern where predominantly the area around the enamel rods are dissolved; and type 3 is a pattern where there is no evidence left of any enamel rods. Besides concluding that type 1 is the most favorable pattern and type 3 the least, the explanation for these different patterns is not known for certain but is most commonly attributed to different crystal orientation in the enamel ^{[46] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_patternexplanation)}.

Tooth Whitening

Tooth whitening, or tooth bleaching, procedures attempt to lighten a tooth's color in either of two ways: by chemical or mechanical action ^{[47] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ada_actions)}.

Working chemically, a bleaching agent is used to carry out an oxidation reaction in the enamel and dentin ^{[48] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summit_oxidation)}. The agents most commonly used are hydrogen peroxide and carbamide peroxide to intrinsically change the color of teeth ^{[49] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summittada_color)}. Enamel can be put at risk to decay/destruction by demineralization if the tooth whitening product has an overall low pH. Consequently, care should be taken and risk evaluated when choosing a product which is very acidic ^{[50] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summitt_acidic)}.

Tooth whiteners in toothpastes work through a mechanical action. They have mild abrasives which aid in the removal of stains on enamel. Although this can be an effective method, the intrinsic color of teeth is not altered ^{[51] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_ada_intrinsiccolor)}.

Microabrasion techniques employ both methods. An acid is used first to weaken the outer 22 - 27 micrometers of enamel in order to weaken it enough for the subsequent abrasive force ^{[52] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_summitt_microabrasion)}. This allows for removal of superficial stains in the enamel. If the discoloration is deeper or in the dentin, tooth whitening will not be successful with this method.

Other anatomical features of enamel

The rod sheath is the border where the crystals of enamel rods and the crystals of interrod enamel meets ^{[53] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_rodsheath)}.

Formed from changes in diameter of Tomes’ processes, striae of Retzius are stripes that appear on enamel when views microscopically in cross-section ^{[54] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_striaeofretzius)}. These stripes demonstrate the growth of enamel similar to the annual rings on a tree. Darker than all the rest, the neonatal line is the stripe that separates the enamel formed before and after birth ^{[55] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cateross_neonatalline)}.

Gnarled enamel is found over the cusps of teeth ^{[56] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_gnarledenamel)}. The twisted appearance results from the orientation of enamel rods and the rows in which they lie.

Perikymata are shallow furrows into which the striae of Retzius end ^{[57] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_perikymata)}.

Enamel Disorders

Amelogenesis imperfecta has many different types. The hypocalcification type, which is the most common, is an autosomal dominant condition resulting in enamel that is not completely mineralized ^{[58] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_harris_hypocalcification)}. Consequently, enamel easily flakes off the teeth, which appear yellow because of the revealed dentin. The hypoplastic type is X-linked and results in normal enamel that appears in too little quantity, having the same effect as the most common type ^{[59] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_harris_hypoplastic)}.

Chronic bilirubin encephalopathy, which can result from erythroblastosis fetalis, is a disease having widespread effects on an infant, but it can also cause enamel hypoplasia and green staining of enamel ^{[60] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_emedicine_erythroblastosis)}.

The term, enamel hypoplasia, is broadly defined to encompass all deviations from normal enamel in its various degrees of absence ^{[61] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_wheelers_enamelhypoplasia)}. The missing enamel could be localized, forming a small pit, or it could be widespread to the point of complete absence.

Erythropoietic porphyria is a genetic disease resulting in the deposition of porphyrins throughout the body. These deposits also occur in enamel and leave an appearance described as red in color and fluorescent ^{[62] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_emedicine_porphyria)}.

Fluorosis leads to mottled enamel and occurs from overexposure to fluoride as explained earlier ^{[63] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_cate_flurosis)}.

Tetracycline staining leads to brown bands on the areas of developing enamel. As a result, tetracycline is contraindicated in pregnant women.

Enamel in non-human Animals

For the most part, research has shown that enamel does not vary consistantly between humans and non-humans. Enamel formation in animals is described almost identically to formation in humans. The enamel organ, including the dental papilla, also function in tooth development as described above, and ameloblasts are the cells which form enamel ^{[64] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_frandson_enamelorgan)}. Instead, the morphology, number, and types of teeth differ more from humans than differences between their enamel. The variations of enamel that are present usually are infrequent but sometimes important.

Dogs are at less risk than humans to have tooth decay. This is due to the very high pH of their saliva, which prevents an acidic environment from forming and the subsequent demineralization of enamel which would occur ^{[65] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_pinney_ph)}. In the event that tooth decay does occur (usually from trauma), dogs receive dental fillings just as humans do. Similar to human teeth, the enamel of dogs are vulnerable to tetracycline staining. Consequently, this risk must be remembered when administering tetracycline antibiotic therapy to young dogs ^{[66] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_pinney_tetracycline)}. Enamel hypoplasia may also occur in dogs ^{[67] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_pinney_hypoplasia)}.

The mineral distribution in enamels of rodents appear differently than that of monkeys, dogs, pigs, and humans ^{[68] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_pubmed_rodent)}. In horse teeth, the enamel and dentin layers are intertwined with each other, which increases the strength and decreases the wear rate of those teeth ^{[69] (http://www.biocrawler.com/encyclopedia/Tooth_enamel#endnote_encartagummed_horse)}.

See also

• Tooth
• Dentin
• Pulp
• Bruxism
• Fluorite
• Ivory
• Keratin
• Elephant and Mammoth ivory
• Walrus ivory
• Perikymata
• Fluoride therapy

References

• American Dental Association, Council on Access Prevention and Interprofessional Relations. "Caries diagnosis and risk assessment: a review of preventive strategies and management." Journal of the American Dental Association, 1995: 126.
• American Dental Association [www.ada.com Website], page on tooth whitening found here (http://www.ada.org/public/topics/whitening_faq.asp)
• American Dental Hygienists' Association. The Oral Health Information page located here (http://www.adha.org/oralhealth/index.html)
• Ash, Major M. and Stanley J. Nelson. Wheeler’s Dental Anatomy, Physiology, and Occlusion. 8th edition. 2003.
• Biology of the Human Dentition (http://www.uic.edu/classes/orla/orla312/BHDTwo.html)
• Cate, A.R. Ten. Oral Histology: development, structure, and function. 5th ed. 1998. ISBN 0815129521.
• Dean, H.T., F.A. Arnold, and E. Elvove. "Domestic water and dental caries." Public Health Reports, 57(32), 1942: pages 1155-79.
• Diagnosis and Managment of Dental Erosion (http://www.thejcdp.com/issue001/gandara/introgan.htm)
• Encarta Online Encyclopedia. "Teeth." Chris Martin. Article found here (http://encarta.msn.com/text_761561931__1/Teeth.html)
• eMedicine homepage (http://www.emedicine.com/)
• Fejerskov, O. Human dentition and experimental animals. Journal of Dental Research. 58, special issue B, March, 1979: pages 725-734. Abstract found at PubMed (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=105027&dopt=Abstract)
• Frandson, R.D. & T.L. Spurgeon. "Anatomy and Physiology of Farm Animals." 5th edition. Philadelphia, Lea & Febiger: 1992. ISBN 0812114353.
• Gandara,B.K. & E.L. Truelove. "Diagnosis and Management of Dental Erosion." The Journal of Contemporary Dental Practice, volume 1 (number 1), October 1999: pages 016-023. Copy of article found here (http://www.thejcdp.com/issue001/gandara/gandara.htm).
• Harris, Edward F. Craniofacial Growth and Development. 2002.
• Newbrun, E. Fluorides and dental caries. 3rd edition. Springfield, Illinois, Charles C. Thomas, publisher: 1986.
• Pinney, Chris C. "The Illustrated Veterinary Guide for Dogs, Cats, Birds, and Exotic Pets." TAB Books, 1992. ISBN 0070501793.
• Randall-Bowman. "Gummed Out: Young Horses Lose Many Teeth, Vet Says." April 2004. Article found here (http://rev.tamu.edu/stories/04/041504-6.html).
• 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.
• Tooth: Structure of a Normal Tooth (http://www.mydr.com.au/default.asp?article=3728)
• Why Teeth Fossilize Better Than Bone (http://www.dinosauria.com/jdp/fossil/teeth.htm)

Notes

1. ^  Ross et al., page 441
2. ^  Cate, page 1
3. ^  Cate, page 219
4. ^  "Biology of the Human Dentition"
5. ^  Cate, page 218
6. ^  "Biology of the Human Dentition"
7. ^  Cate, page 198
8. ^  "Biology of the Human Dentition"
9. ^ Ross et al., page 441
10. ^  Cate, page 219; Ross et al., page 441
11. ^  Ross et al., page 441
12. ^  Cate, page 224
13. ^  Cate, page 224
14. ^  Cate, page 219
15. ^  Ross et al., page 443
16. ^  Cate, page 224
17. ^  Cate, page 197
18. ^  Ross et al., page 445
19. ^  Cate, page 208
20. ^  Ross et al., page 445
21. ^  Ross et al., page 447
22. ^  Ross et al., page 448
23. ^  Ross et al., page 3
24. ^  American Dental Hygienists' Association, accessed here (http://www.adha.org/oralhealth/whitening.htm)
25. ^  Summit et al., page 2
26. ^  Summit et al, page 2
27. ^  Ash & Stanley, page 54
28. ^  Ross et al., page 443
29. ^  Ross et al., page 453
30. ^  Ross et al., page 453
31. ^  Gandara & Truelove. Information found on chart titled, "Definitions of Tooth Surface Loss," and the specific page can be accessed here (http://www.thejcdp.com/issue001/gandara/introgan.htm).
32. ^  Dean et al.
33. ^  Cate, page 223
34. ^  Ross et al., page 453
35. ^  Cate, page 216
36. ^  American Dental Association
37. ^  Newbrun, 1986
38. ^ Summitt, et al., page 273
39. ^ Summitt et al., page 274
40. ^  Summitt et al., page 7
41. ^  Summitt et al., page 191
42. ^  Cate, page 233
43. ^  Summitt et al., page 193
44. ^ Summitt et al., page 193
45. ^  Summitt et al., page 193
46. ^  Cate, page 235
47. ^  American Dental Assocation's whitening page found here (http://www.ada.org/public/topics/whitening_faq.asp)
48. ^  Summit et al., page 402
49. ^  American Dental Assocation's whitening page notes the intrinsic change and can be accessed here (http://www.ada.org/public/topics/whitening_faq.asp), and Summit et al.lists the two most common agents, page 403
50. ^  Summitt et al., page 404
51. ^  American Dental Assocation's whitening page found here (http://www.ada.org/public/topics/whitening_faq.asp)
52. ^ Summitt et al., 420
53. ^  Cate, 221
54. ^  Cate, 224
55. ^  Cate, page 76; Ross et al., page 441
56. ^  Cate, page 229
57. ^  Cate, page 230
58. ^  Harris, page 7 in section titled, "X-Linked Inheritance"
59. ^  Harris, page 7 in section titled, "X-Linked Inheritance"
60. ^  eMedicine on erythroblastosis fetalis, page accessed [here (http://www.emedicine.com/ped/topic1247.htm)]
61. ^  Ash & Stanley, page 31
62. ^ eMedicine on porphyria, page accessed [here (http://www.emedicine.com/derm/topic145.htm)]
63. ^  Cate, page 216
64. ^  Frandson & Spurgeon, page 305
65. ^  Pinney, page 187
66. ^  Pinney, page 187
67. ^  Pinney, page 186
68. ^  Fejerskov, O. on Pubmed. Link can be found here (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=105027&dopt=Abstract)
69. ^  Encarta article found here (http://encarta.msn.com/text_761561931__1/Teeth.html) and Randall-Bowman, whose link can be found here (http://rev.tamu.edu/stories/04/041504-6.html)eo:Emajlo (dento)

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