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Twenty-five permanent premolars were evaluated for enamel defects. The primary molars that they succeeded had been successfully treated with a formocresol pulpotomy. A relationship between the enamel defects and the pulpotomy procedures has been found.
The rare variant of opalescent dentin associated with enamel defect was found in a 1 1/2-year-old boy. The pulp chambers and root canals of the affected deciduous teeth were very large, with no sign of obliteration. The enamel layer of those teeth was markedly reduced in thickness, and the enamel prisms were not recognized even by scanning electron microscopy. The mantle dentin was abnormal, as were other portions of dentin.
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Ameloblastic disturbances are correlated with defects in enamel. Experimental disturbances created by tetracyclines, fluorides, and antimitotic drugs are emphasized. Cellular alterations are shown to interfere with both matrix production and secretion. Defects in enamel formation are characterized by abnormal crystal size and distribution. Further research in normal and particularly abnormal enamel development is needed to establish: 1. exact mode of matrix secretion and its relation to crystal nucleation and orientation 2. function of maturative ameloblast and its relation to the stratum intermedium and papillary layer during that phase 3. cause for lack of mineralization of matrix, particularly in ectopic areas.
We conducted a multi-ancestry genome-wide association study (GWAS) of developmental defects of enamel (DDE) in the primary dentition among 6,061 U.S. preschool-aged children (3-5 years). We investigated four DDE phenotypes (demarcated opacities, diffuse opacities, hypoplastic defects, and a combined DDE trait) leveraging main-effect models, joint gene-sex interaction testing (2df), and sex-stratified analyses. SNP-based heritability for the combined DDE trait was estimated at 20%, with concordance analyses robustly supporting a genetic etiology. We identified 39 unique genome-wide significant loci (P<5×10 ), with five surpassing a study-wide Bonferroni-corrected statistical significance criterion (P<1.25×10 9), including Y RNA and ALDH1A1. The main-effect GWAS identified 20 loci, including HBS1L and MYB, genes regulating hematopoiesis with plausible roles in amelogenesis. Joint test and sex-stratified analyses revealed 19 additional loci, including ALDH1A1, TENM2, and DLGAP2, demonstrating sex-specific heterogeneity. Nineteen loci exhibited sex-specific differences after Bonferroni correction (P<2x10-3), including genes involved in retinoic acid signaling (ALDH1A1), odontogenesis (TENM2), and neurodevelopment (DLGAP2, CDH10). Pathway enrichment highlighted ectodermal and synapse organization networks, suggesting shared etiological mechanisms between DDE and systemic conditions like neurofibromatosis and autism spectrum disorder. Notably, no locus generalized in an external GWAS of permanent dentition DDE, underscoring fundamental biological differences in the genetic architectures governing primary versus permanent enamel formation. Crucially, a comprehensive cross-trait pleiotropy lookup against early childhood caries (ECC) revealed no shared genetic architecture, supporting the notion that the established clinical and epidemiological association between DDE and ECC is likely driven by structural defects increasing caries lesion susceptibility rather than genetic pleiotropy. By integrating gene-sex interaction testing, this study offers novel insights into the complex, sexually dimorphic genetic etiology of DDE and augments the biological evidence base that can support the development of precision pediatric dentistry.
The nature of the enamel defects in a patient with epidermolysis bullosa hereditaria dystrophica was observed by light microscopy, microradiography, and scanning electron microscopy (SEM) so that by these means more detailed information could be obtained. The random distribution of the round shape of the hypoplastic defects of enamel with hypomineralization, in which there is a continuity of the incremental lines, suggested the possibility that some ameloblasts maintained hypoactivity of their secretory function during their total life span.
Linear hypoplasia of the deciduous teeth is rare in most human populations, but common where nutritional status is poor. Deciduous enamel hypoplasia, hypocalcification, and hypoplasia-related caries are described in Middle and Late Woodland skeletal series from the Lower Illinois Valley. Gross enamel defects that can be referred to pre-natal development are found in 83 of 170 children under six years of age at death. Circular caries secondary to hypoplasia is significantly more common in the Late Woodland series, reflecting the apparent higher cariogenicity of Late Woodland diets. There is a significant association between prenatal dental defects and bony evidence for anemia and infectious disease. Children with enamel defects show relatively higher weaning age mortality than those without. These relationships suggest that at least moderate levels of malnutrition existed in Illinois Woodland populations.
An aluminum plant on the south bank of the St. Lawrence river, southwest of Cornwall Island, Ontario, Canada, has emitted 0.816 metric tons of fluoride daily since 1973; considerably higher amounts were emitted from 1959 to 1973. The plant has been designated as the "major source of fluoride emissions impacting on Cornwall Island." Chronic fluoride poisoning in Cornwall island cattle was manifested clinically by stunted growth and dental fluorosis to a degree of severe interference with drinking and mastication. Cows died at or were slaughtered after the third pregnancy. The deterioration of cows did not allow further pregnancies. Fluoride concentrations in ash of biopsied coccygeal vertebrae increased significantly with age and were dependent on distance from and direction to the aluminum plant. Fluoride in bone ash of a 7-month old-fetus exceeded 500 ppm; fluoride thus was passed transplacentally. Analyses of fluoride in ash of bones obtained at necropsy of cattle from 4 months of age to 4 to 5 years of age showed increased amounts with age. Cancellous bone retained far higher amounts than cortical bone, a reflection of the normally higher metabolic rate of cancellous bone. Concentrations exceeding 10,000 ppm fluoride were recorded in cancellous bone of a 4-to 5-year-old cow. The target cells for fluoride in chronic fluorosis were shown to be the ameloblasts, the dental pulp cells and the odontoblasts and, in bone, primarily the resorbing osteocytes and also the osteoblasts. Atrophy and necrosis of the ameloblasts were responsible for enamel defects. The existing enamel showed brown discoloration from fluoride deposits. The pulp cells underwent fibrous and osseous metaplasia and necrosis of the ectopic bone occurred. The odontoblasts were atrophic and the dentin showed brown discoloration. The resorbing osteocytes were inactive and osteosclerosis resulted. This was especially pronounced in areas of normally great apposition, i.e. in the metaphyses. The epiphyseal plate became squeezed between petrotic bone and growth was stunted. Resorption of alveolar bone surrounding the deciduous teeth was severely retarded or arrested. A delay in eruption of permanent teeth occurred; it was up to 3.5 years in incisor teeth. Interference with the resorbing osteocytes in fluorotic bone was also demonstrated by loss of collagen birefringency in such bone. Failure of bone resorption also caused retention of trabecular bone in the cortices; this was observed even in a 4-t0-5-year-old cow. In areas where modeling into osteonic bone had begun, fluoride deposits were extremely heavy but this bone showed numerous soft osteons in microradiographs. The toxic effect of fluoride on osteocytes also resulted in the death of the cells. Such osteonecrosis occurred mainly in gnathic bone. There was atrophy of the osteoblasts. Osteopenia thus resulted from osteonecrosis and osteoporosis. Subperiosteal exostoses were not observed in long bones. The degree of fluorosis in Cornwall Island cattle was severe...
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Defects of the enamel include hypoplasia and hypomineralization. The cause can be local, systemic, or hereditary. A 14-year-old boy had type 4 hereditary hypoplastic enamel. The Nuva-Seal, Nuva-Fil acid-etch technique was used to restore the defect.
It could be demonstrated that enamel defects which are caused by maxillo-facial fixing elements of actively removable implements were reproducible in laboratory experiments. With minimal pressure of the wire bow of 50 grams and 250,000 lift, or individual vertical movements on the enamel surface resulted in a micrometer area of scouring.
The association of taurodontism with hypoplastic/hypomature enamel defects is presented in two cases of X-chromosome aneuploidy (47,XXY) and one of X-linked recessive Amelogenesis Imperfecta. It appears that the X-chromosome not only plays some role in tooth size the degree of taurodontism increasing with increased number of X chromosomes), but probably also plays a role in enamel maturation.
Two brothers showed severe and persistent hyperchloraemic metabolic acidosis (capillary blood pH 7.07--7.15) due to a low renal bicarbonate threshold at 11 mmol/l. The maximal tubular capacity for bicarbonate reabsorption was reduced to about half the normal. A high dose of acetazolamide (25 mg/kg) lowered the tubular bicarbonate reabsorption substantially, indicating the presence of carbonic anhydrase. Both the glomerular filtration rate, the renal blood flow and the renal concentrating capacity were slightly reduced. The clinical characteristics were: growth retardation, mental retardation, nystagmus, corneal opacities, cataract, glaucoma and enamel defects of the permanent teeth. Serum thyroxine was pathological low without clinical signs of hypothyreosis. The erythrocytes showed an increased osmotic resistance. Autopsy of the younger brother, who died 4 1/2 years old, revealed thyroid and thymus weights of 25% of the normal. The kidney tubular cells were swollen with vacuoles. The glomeruli had a normal appearance.
The affected teeth in this case of odontodysplasia exhibited abnormal hypoplastic enamel, abnormal dentin containing extensive interglobular regions and completely lacking a peritubular matrix, and an abnormal irregular tissue consisting of highly calcified and partially fused granules located within the dentin of the tooth tips. Electron micrographs of the irregular tissue showed that the granules consisted of crystallites densely and radically packed in a noncollagenous amorphous matrix. Granules were surrounded by a slightly calcified, irregularly arranged, collagenous matrix. The irregular tissue formed in the pulp of the tooth tip befofe and independently of the dentin. It was at least partially formed by pulpal calcification. Abnormal dentin matrix was formed by odontoblasts which were less differentiated than normal. Odontodysplastic teeth showed abnormal differentiation of odontoblasts and ameloblasts resulting in defective enamel and dentin and, in extreme cases, in extensive pulpal calcification.
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