Molars that are malformed due to enamel hypoplasia, enamel hypocalcification, or amelogenesis imperfecta routinely challenge dentists who treat children A tooth which has been disturbed during its formation may develop atypical or abnormal enamel. This is usually seen as a white, yellow, or brown discoloration . What is enamel hypocalcification? Enamel hypocalcification (sometimes mistakenly called enamel hypoplasia) is a condition where the enamel does not form.
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Dental fluorosis also termed mottled enamel  is an extremely common  disorder, characterized by hypomineralization of tooth enamel caused by ingestion of excessive fluoride during hypoalcification formation. It appears as a range of visual changes in enamel  causing degrees of intrinsic tooth discolorationand, in some cases, physical damage to the teeth.
The severity of the condition is dependent on the dose, duration, and age of the individual during the exposure. In the “mild” form of the disease, these mottled patches can involve up to half of the surface area of the teeth. When fluorosis is moderate, all of the surfaces of the teeth are mottled and teeth may be ground down and brown stains frequently “disfigure” the teeth. Severe fluorosis is characterized by brown discoloration and discrete or confluent pitting; brown stains are widespread and teeth often present a corroded-looking appearance.
People with fluorosis are relatively resistant to dental caries tooth decay caused by bacteria although they may be of cosmetic concern. The adequate diagnosis of fluorosis hypocalciication be diagnosed by visual enamsl examination. This requires inspection of dry and clean tooth surfaces under a good lighting. There are different classifications to diagnose the severity based on the appearances.
In dental enamel, fluorosis causes subsurface porosity or hypomineralizations, which extend toward the dentinal-enamel junction as severity increases. Hence, affected teeth are more susceptible to staining. Due to diffusion of exogenous ions ex, iron and copperthe stains would develop into the abnormally porous enamel.
The differential diagnosis for this condition includes:. The two main classification systems are described below. Others include the tooth surface fluorosis index Horowitz et al. Dean’s fluorosis index was first published in by H.
The index underwent two changes, appearing in its final form in Proposed by Thylstrup and Fejerskov inthe TF index represents a logical extension of Dean’s index, incorporating modern understanding of the underlying pathology of fluorosis.
Dental fluorosis is caused by a higher than normal amount of fluoride ingestion whilst teeth are forming.
Dental fluorosis – Wikipedia
Primary dentine fluorosis and enamel fluorosis can only happen during tooth formation, so fluoride exposure occurs in childhood. Enamel fluorosis has a white opaque appearance which is due to the surface of the enamel being hypomineralised. The most superficial concern in dental fluorosis is aesthetic changes in the permanent dentition the adult teeth. The period when these teeth are at highest risk of developing fluorosis is between when the child is born up to 6 years old, though there has been some research which proposes that the most crucial course is during the first 2 years of the child’s life.
Dental fluorosis has been growing in the United States concurrent with fluoridation of municipal water supplies, although disproportionately by race. Teeth are the most studied body tissues to examine the impact of fluoride to human health.
There are a few possible mechanisms that have been proposed. It is generally believed that the hypomineralization of affected enamel is mainly due to in-situ toxic effects of the fluoride on the ameloblasts in the enamel formation, and not caused by the general effects of fluoride on the calcium metabolism, or by the poisoning effects that suppress the fluoride metabolism. However, despite decades of research and studies, there have yet to be any studies that substantiates the believed mechanism whereby dental fluorosis is a result of alteration in the mineralisation that takes place when fluroide interacts with mineralising tissues.
In the extra-cellular environment of maturing enamel, an excess of fluoride ions alters the rate at which enamel matrix proteins amelogenin are enzymatically broken down and the rate at which the subsequent breakdown products are removed.
This hypomineralized enamel has altered optical properties and appears opaque and lusterless relative to normal enamel. Traditionally severe fluorosis has been described as enamel hypoplasiahowever, hypoplasia does not occur as a result of fluorosis. Hydroxyapatite is converted to fluorohydroxyapatite as follows:.
Dental fluorosis may or may not be of cosmetic concern. In some cases, there may be varying degrees of negative psychosocial effects. The treatment options are:.
Before the study was published, CDC published an interim report covering data from to Centers for Disease Control found a 9 percentage point increase in the prevalence of confirmed dental fluorosis in a study of American children and adolescents than was found in a similar survey from from In addition, the survey provides further evidence that African Americans suffer from higher rates of fluorosis than Caucasian Americans.
The condition is more prevalent in rural areas where uypocalcification water is derived from shallow wells or hand pumps. It is thus improbable a person will receive more than the tolerable upper limit from consuming optimally fluoridated water alone. Fluoride consumption can exceed the tolerable upper limit when someone drinks a lot of fluoride-containing water in combination with other fluoride sources, such as swallowing fluoridated toothpaste, consuming food with a high fluoride content, or consuming fluoride supplements.
The use of fluoride supplements as a prevention for tooth decay is rare in areas with water fluoridation, but was recommended by many dentists in the UK until the early hypkcalcification.
Dental fluorosis can be prevented hypocalcificatioj lowering the amount of fluoride intake to below the tolerable upper limit. In November the American Dental Association published information stating that water fluoridation is safe, effective and healthy; that enamel fluorosis, usually mild and difficult for anyone except a dental health care professional to see, can result from ingesting more than optimal amounts of fluoride in early childhood; that it is safe to use fluoridated water to mix infant formula; and that the probability of babies developing fluorosis can be reduced by using hypocalciication infant formula or using water that is either free of fluoride or low in fluoride to prepare powdered or liquid concentrate formula.
They go on to say that the way to get the benefits of fluoride but minimize the risk of fluorosis for a child is to get the right amount of fluoride, not too much and not too little. In ancient times, Galen describes what is thought to be dental fluorosis. In Eager published the first description of the “mottled enamel” of immigrants from a small village near Naples, Italy. After examining specimens of affected enamel, in Black described the condition as “[a]n endemic imperfection of the enamel of the teeth, heretofore unknown in the literature of dentistry.
In3 different groups of scientists around the world published their discoveries that this condition was caused by fluoride in drinking water during childhood. From Wikipedia, the free encyclopedia. Dental fluorosis Mild fluorosis: Oral and Maxillofacial Pathology 4th ed.
The Cochrane Database of Hypoca,cification Reviews 1: Early Childhood Oral Health. The History of Fluorine, Fluoride and Fluoridation. Retrieved 12 November Journal of Esthetic and Restorative Dentistry. The Disease and Its Clinical Management.
Health effects of ingested fluoride. Monographs in Oral Science. Community Dentistry and Oral Epidemiology. Fluoride intake of children: Fluoride in Drinking-water PDF. D; Barker, L; Dye, B. NCHS data brief Journal of dental hygiene: Archived PDF from the original on Centers for Disease Control and Prevention.
Reprinted in “Public Health Reports, November 1, Denti di Chiaie Chiaie teethby J. Bull Acad Vet France. The National Medical Journal of India.
Archived from the original PDF on Oral and maxillofacial pathology K00—K06, K11—K14—, — Bednar’s aphthae Cleft palate High-arched palate Palatal cysts of the newborn Inflammatory papillary hyperplasia Stomatitis nicotina Torus palatinus. Oral mucosa — Lining of mouth.
Squamous cell papilloma Keratoacanthoma Malignant: Adenosquamous carcinoma Basaloid squamous carcinoma Mucosal melanoma Spindle cell carcinoma Squamous cell carcinoma Verrucous carcinoma Oral florid papillomatosis Oral melanosis Smoker’s melanosis Pemphigoid Benign mucous membrane Pemphigus Plasmoacanthoma Stomatitis Aphthous Denture-related Herpetic Smokeless tobacco keratosis Submucous fibrosis Ulceration Riga—Fede disease Verruca vulgaris Verruciform xanthoma White sponge nevus.
Enamel hypocalcification – Wikipedia
Periodontium gingivaperiodontal ligamentcementumalveolus — Gums and tooth-supporting structures. Cementicle Cementoblastoma Gigantiform Cementoma Eruption cyst Epulis Pyogenic granuloma Congenital hypoczlcification Gingival enlargement Gingival cyst of the adult Gingival cyst of the newborn Gingivitis Desquamative Granulomatous Plasma cell Hereditary gingival fibromatosis Hypercementosis Hypocementosis Linear gingival erythema Necrotizing periodontal diseases Acute necrotizing ulcerative gingivitis Pericoronitis Peri-implantitis Periodontal abscess Periodontal trauma Periodontitis Aggressive As hypocalcificatiion manifestation of systemic disease Chronic Perio-endo lesion Teething.
Periapical, mandibular and maxillary hard tissues — Bones of jaws. Nasopalatine duct Median mandibular Median palatal Traumatic bone Osteoma Osteomyelitis Osteonecrosis Bisphosphonate-associated Neuralgia-inducing cavitational osteonecrosis Osteoradionecrosis Osteoporotic bone marrow defect Paget’s disease of bone Periapical abscess Phoenix abscess Periapical periodontitis Stafne defect Torus mandibularis.
Temporomandibular jointsmuscles of mastication and malocclusions — Jaw joints, chewing muscles and bite abnormalities. Benign lymphoepithelial lesion Ectopic salivary gland tissue Frey’s syndrome HIV salivary gland disease Necrotizing sialometaplasia Mucocele Ranula Pneumoparotitis Salivary duct stricture Salivary gland aplasia Salivary gland atresia Salivary gland diverticulum Salivary gland fistula Salivary gland hyperplasia Salivary gland hypoplasia Salivary gland neoplasms Benign: Basal cell adenoma Canalicular adenoma Ductal papilloma Monomorphic adenoma Myoepithelioma Oncocytoma Papillary cystadenoma lymphomatosum Pleomorphic adenoma Sebaceous adenoma Malignant: Orofacial soft tissues — Soft tissues around the mouth.
Eagle syndrome Hemifacial hypertrophy Facial hemiatrophy Oral manifestations of systemic disease. Retrieved from ” https: Developmental tooth disorders Toxic effects of dietary elements.
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