Understanding Environmental Enamel Hypoplasia

Understanding Environmental Enamel Hypoplasia

Question. Describe environmental enamel hypoplasia.

Answer. Environmental enamel hypoplasia may be defined as an incomplete or defective formation of the organic enamel matrix of teeth.

• Enamel hypoplasia (EH) is a quantitative defect associated with a reduced localized thickness of enamel, following disruption of the secretory phase of amelogenesis.
• The enamel may be translucent or opaque, with single or multiple pits or grooves and partial or complete absence of enamel over significant areas of dentin. The enamel hypoplasia defects tend to occur in the incisal or cuspal one­third of the crown.
• A defect that is caused by environmental factors, either dentition may be involved and sometimes only a single tooth; both enamel and dentin are usually affected, at least to some degree.
• It is known that many different factors, each capable of producing injury to the ameloblasts, may give rise to the condition, including:

“Common challenges in diagnosing environmental enamel hypoplasia effectively: FAQs provided”

• • Nutritional deficiency (vitamins A and D)
  • Exanthematous diseases (e.g. measles, chickenpox, scarlet fever)
  • Congenital syphilis
  • Hypocalcemia
  • Birth injury, Prematurity and Rh hemolytic disease
  • Local infection or trauma
  • Ingestion of chemicals (chiefl floride)
  • Idiopathic

“Understanding environmental enamel hypoplasia through FAQs: Q&A explained”

• In mild environmental hypoplasia, there may be only a few small grooves, pits, or fisures on the enamel surface.
  If the condition is more severe, enamel may exhibit rows of deep pits arranged horizontally across the surface of the tooth.
  There may be only a single row of such pits or several rows indicating a series of injuries.
• In most severe cases, a considerable portion of enamel may be absent, suggesting a prolonged disturbance in the function of the ameloblasts.
• Hypoplasia results only if the injury occurs at the time teeth are developing, or more specifially during the formative stage of enamel development.
  Once the enamel has calcifid, no such defect can be produced.
  Thus, knowing the chronologic development of the deciduous and permanent teeth,it is possible to determine from the location of the defect on the teeth the approximate time at which the injury occurred.

“Importance of studying environmental enamel hypoplasia for better diagnostic outcomes: Questions explained”

Enamel Hypoplasia Due to Vitamin A Defiiency

Although tissues of ectodermal origin i.e., the epidermis is primarily affcted in vitamin A defiiency, teeth also record this defiiency.

Avitaminosis A is evidenced by marked metaplasia of the enamel organ, which results in defective enamel formation.

This view originates from histological changes seen initially in the oral mucosa and extending to the degeneration of the epithelial­derived ameloblasts, which results in a hypoplastic enamel matrix.

If vitamin A defiiency is severe,ameloblast cells will become completely atrophied, which results in an absence of enamel formation.

In less severe cases, the columnar ameloblasts apparently shorten, and adjacent enamel exhibits hypoplasia.

If vitamin A defiiency is relieved during subsequent tooth development, normal enamel is produced,although defective tissue is not repaired.

“Factors influencing success with environmental enamel hypoplasia treatment: Q&A”

Enamel Hypoplasia Due to Vitamin D Defiiency

Vitamin D is essential for deposition of calcium and phosphorus in hard tissues.

Its presence increases the absorption of dietary calcium and maintains proper levels of calcium and phosphorus in the blood.

Primary defiiency of vitamin D results from insuffient exposure to the sun and insuffient dietary intake.

Secondary defiiencies result from abnormal intestinal resorption.

Secondary defiiencies may be overcome by alteration of dietary intake of calcium and phosphorus.

A severe vitamin D defiiency in children results in rickets, a condition characterized by insuffient deposition of calcium salts in bony tissue.

Dental features of rickets include enamel hypoplasia due to failure of tooth mineralization. Enamel hypoplasia is of pittd type.

“Steps to explain causes of environmental enamel hypoplasia: Nutritional deficiencies vs infections: Q&A guide”

Enamel hypoplasia Due to exanthematous Diseases

Some studies have indicated that exanthematous diseases,including measles, chickenpox and scarlet fever, are etiologic factors.

In general, it might be stated that any serious nutritional deficiency or systemic disease is potentially capable of producing enamel hypoplasia, since ameloblasts are one of the most sensitive groups of cells in body in terms of metabolic function.

The type of hypoplasia occurring from these defiiency or disease states is usually of the pittng variety.

Since the pits tend to stain, the clinical appearance of the teeth may be very unsightly.

Clinical studies indicate that most cases of enamel hypoplasia involve those teeth that form within the fist year after birth, although teeth that form somewhat later may be affcted.

Thus the teeth most frequently involved are the central and lateral incisors, cuspids and fist molars.

“Role of malnutrition in causing environmental enamel hypoplasia: Questions answered”

Enamel Hypoplasia Due To Congenital Syphilis

Congenital syphilis arises from transplacental fetal infection with Treponema pallidium acquired during pregnancy from an untreated mother.

The disease is divided into an early stage that usually occur before 3 months, but may be seen up to 2 years, and late stage disease that occurs after 2 years.

Late congenital syphilis affct the amelogenesis of the molars and incisors.

Both Hutchinson teeth and mulberry molars are seen in about 65% of patients.

These characteristic teeth present at around 6 years; they are centrally notched, widely spaced, peg­shaped upper permanent central incisors.

Patients with congenital syphilis may also have mulberry molars, which are fist molars dwarfed by a small occlusal surface, and are characterized by roughened lobulated hypoplastic enamel leading to caries.

The surface has numerous poorly formed cusps which overcome to form a dome­shaped tooth, which is considerably narrower at the grinding surface than at its base.

“Early warning signs of issues addressed by understanding environmental enamel hypoplasia pathogenesis: Common questions”

Enamel Hypoplasia Due To Hypocalcemia

Tetany induced by a decreased level of calcium in the blood, may result from several conditions, the most common being vitamin D deficiency and parathyroid deficiency (parathyroprivic tetany).

In tetany the serum calcium level may fall as low as 6–8 mg per l00 mL, and at this level enamel hypoplasia is frequently produced in teeth developing concomitantly This type of enamelhypoplasia is usually of the pittng variety and thus does not diffr from that resulting from a nutritional disturbance or exanthematous disease.

Enamel Hypoplasia Due To Birth Injuries

The neonatal line or ring, described by Schour in 1936 and present in deciduous teeth and fist permanent molars, may be thought of as a type of hypoplasia because there is a disturbance produced in the enamel and dentin, which is indicative of trauma or change of environment at the time of birth.

“Asymptomatic vs symptomatic effects of ignoring environmental enamel hypoplasia causes: Q&A”

Enamel Hypoplasia Due To Local Infection Or Trauma

A type of hypoplasia occasionally seen is unusual in that only a single tooth is involved, most commonly one of the permanent maxillary incisors or a maxillary or mandibular premolar.

There may be any degree of hypoplasia, ranging from a mild, brownish discoloration of the enamel to a severe pittng and irregularity of the tooth crown.

Another frequent pattrn of enamel defects seen in permanent teeth is caused by periapical inflmmatory disease of the overlying deciduous tooth. The altered tooth is called Turner’s tooth.