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Biomedical subjects

H Weyers

Publications and source records attributed to H Weyers.

At least 19 recordsLinked to original sources
PubMed1980

[Atypical diastemas in the anterior region of the jaws].

Familial occurrence of diastemas in the pericanine region of the maxilla and mandible was described which differs from known localizations. Postcanine occurrence was found in the maxilla; precanine occurrence, in the mandible. This therefore differs from phylogenic diastemas, such as the diastemas in the deciduous dentation of monkeys and primates. Reasons for the influence of local disturbances (e.g., aplasia, dystopia, persistence of embryofetal frenula) could not be determined; ritual (traumatic) mutilation could also be excluded.

Cuspid↗
PubMed1980

[Aplasia of the premolars as a leading symptom of ectodermal dysplasia].

The primary symptom in the tooth system, a tendency toward aplasia of the bicuspid teeth in both dentition periods, was reported for an ectodermal syndrome which has seldom been described. In agreement with the observation by BOOK (1950), we also observed excessive perspiration (hyperhidrosis) and premature graying of the scalp hair (canities prematura). The syndrome, which is limited to ectodermal disturbances, is a dominant trait, the incidence of which is apparently higher in Northern European countries. Trigeminal neuralgias seem to appear in conjunction with this genetic disturbance. Compared with other partial anodontic and oligodontic syndromes, it is striking that no other groups of teeth are affected; the bicuspid teeth however show signs of aplasia, hypoplasia, structural disturbances (discoloration), and premature loss of even the deciduous teeth.

Bicuspid↗
PubMed1977

[A particular type of dominant hereditary enamel dysplasia?].

An enamel dysplasia which is obviously transmitted as a dominant trait, is observed in various members of one family over three generations. The picture of affected and non-affected teeth of both dentitions is different from the usual behavior of generalized enamel hypoplasia, as only a delimited period of enamel formation is affected. Findings of exogenous inflammatory changes in enamel make the nature of this hereditary odontopathia more understandable. The origin of this enamel hypoplasia is supposed to be a genetic phase-specific process in the stage of maximum metabolic activity (enamel formation). In different age groups, this disorder shows different degrees of severity, suggesting the existence of modifying factors. Among the subjects, the male sex is predominant, while the females exhibit more marked hypoplasias. Whether this is a new variant of hereditary dusturbance of enamel formation can be confirmed by examination of other large families.

Amelogenesis Imperfecta↗