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PubMed1997

Expression of osteocalcin in cementoblasts forming acellular cementum.

To determine the phenotypic expression of cementoblasts responsible for acellular cementum, an immunohistochemical study was performed using a polyclonal antibody raised against the aminoterminal peptide of rat osteocalcin (OC). Maxillary first molars of Wistar male rats aged 2 and 3 wk were used for observations. Serial sections of decalcified paraffin embedded specimens were stained either with hematoxylin and eosin or with the anti-OC antibody. In 2-wk-old rats, apical roots were lined with the epithelial root sheath. A thin layer of acellular cementum was seen at most of the root surface, but was not seen near to root apex. In 3-wk-old rats, cellular cementum began to be formed at root apex, and acellular cementum became more thick than in 2-wk-old rats. Acellular and cellular cementum were lined with the fibroblast-like cells. Osteocalcin staining was detected in cells lining root surface in both 2- and 3-wk-old rats. Almost all cells lining cellular cementum were positive for OC. In contrast OC positive cells lining acellular cementum and root surface devoid of cementum appeared at a specific site of the root. The cells at the interradicular area of root surface were positive but the cells at the outer area (the opposite side of the interradicular area) were negative for OC. Osteoblasts and odontoblasts were positive with the antibody. The present results suggest that the OC expression of cementoblasts forming acellular cementum is similar to that of cells forming cellular cementum as well as osteoblasts and odontoblasts, and has a role for calcification of acellular cementum.

Animals↗
PubMed1999

[Relationships between mandibular canine calcification stages and skeletal maturity].

OBJECTIVE: To study the relationship between mandibular canine calcification and skeletal maturity. METHODS: Hand wrist and mandibular canine radiographs of 106 boys and 152 girls in Beijing area were assessed. RESULTS: Mandibular canine calcification coincides with the initiation of puberty in male (93.8%) and with the deceleration of puberty in female(89.7%). However the coincidence with the indicators of other pubertal stages was less than 50%. CONCLUSION: Mandibular canine calcification just can give an initial assessment for estimating the timing of puberty.

Adolescent↗
PubMed1986

Ca-ATPase and ALPase activities at the initial calcification sites of dentin and enamel in the rat incisor.

Enzymatic activities of calcium-magnesium dependent adenosine triphosphatase (Ca-ATPase) and nonspecific alkaline phosphatase (ALPase) were localized at the initial calcification sites of dentin and enamel of rat incisor teeth using electron-microscopic cytochemistry. Ca-ATPase was localized in the Golgi cisternae, cytoplasmic vesicles and along the outer surface of the presecretory and secretory ameloblasts, whereas it was totally absent from the odontoblasts in the pulp. Inversely, ALPase reaction was localized along the outer surface of the odontoblasts, but almost completely absent from the ameloblasts. Diffuse extracellular reactions of both enzymes were distributed throughout the unmineralized fibrous matrix of mantle dentin in which a large number of matrix vesicles were scattered. Both Ca-ATPase and ALPase reactions, which appeared in the matrix vesicles in the process of formation of mantle dentin, became most conspicuous at the site of initial dentin calcification. At this stage, an intense Ca-ATPase reaction also appeared along some of the collagen fibrils adjacent to the reactive matrix vesicles. No ALPase reaction was localized along these Ca-ATPase reactive collagen fibrils. Our observations suggest strongly that Ca-ATPase in the matrix vesicles originates from the inner enamel epithelium and/or preameloblasts whereas ALPase originates from the odontoblasts in the pulp. The importance of the coexistence of both enzymes for the control of initial calcification of dental hard tissues is suggested.

Alkaline Phosphatase↗
PubMed1994

Delayed calcification and congenitally missing teeth. Case report.

A case of delayed differentiation and/or calcification, that is, development, followed by accelerated growth of the maxillary second premolars is presented. This condition was accompanied by the congenital absence of mandibular second premolars even though maxillary and mandibular third molar germs were present. The case was followed over a five-year period. It seems that agenesis of any tooth might be found in conjunction with delay in development of any other tooth. Moreover, full development of a tooth germ (followed by an accelerated growth) as well as pathological changes may occur, despite an initial marked delay in tooth development.

Anodontia↗
PubMed1979

Phosphopeptides of enamel matrix.

Although the tripeptides Glu-O-Phosphoserine-Tyr and Glu-O-Phosphoserine-Leu have been identified in embryonic bovine enamel proteins, 1, 2 the issue of whether both sequences occur in each of the phosphopeptides, or whether certain sequences occur in specific peptides only, has recently been resolved by isolating homogeneous samples of E33 and E44. All three of the Ser residues of both peptides are phosphorylated. All three in E3 are in the sequence Glu-O-Phosphoserine-Leu, and all three in E4 are in the sequence Glu-O-Phosphoserine-Tyr. It was not possible to sequence either of the polypeptide chains directly by automatic peptide sequencing. However, a partial sequence of E4 was constructed from data derived from peptides isolated after cyanogen bromide, trypsin and chymotrypsin digestions. The presence of Glu, Tyr and Leu adjacent to and near the O-Phosphoserine [Ser(L)] residues and the 2 degrees, 3 degrees and higher ordered structures of the enamel phosphopeptides may be important in calcium binding and mineralization.

Amino Acid Sequence↗
PubMed1984

Dysplastic enamel in odontoma: a light microscopic, microradiographic and SEM study.

Dysplastic enamel and calcifications at the enamel surface in 7 odontomas were studied, using correlated light microscopy of decalcified and undecalcified material, microradiography and SEM. Much of the dentin in the odontomas was not covered with enamel. When present, the enamel was immature and assumed a prismatic structure. The prisms were irregular distributed and associated with spherical calcifications. The calcifications adhering to the enamel surface or separated from it presented variations in size, morphology, staining reactions and radiodensity. The correlated techniques of light microscopy, microradiography and SEM indicated that all the calcifications adhering to the enamel surface and part of those separated from it may be related to a pathological process of amelogenesis. Most of the calcifications separated from enamel and often formed around nidi of ghost cells, are the result of a dystrophic mineralizing process, definitely distinct from amelogenesis.

Calcinosis↗
PubMed1981

Transmission electron microscopy of reparative dentin in rat molar pulps. Primary mineralization via extracellular matrix vesicles.

A reparative dentin bridge was induced in rat molar teeth by pulp exposure and capping with calcium hydroxide. Transmission electron-microscopic examination after 10 days revealed the presence of odontoblastic cells and collagenous matrix with focal calcifications. The calcifying fronts were composed of hydroxyapatite crystals. Numerous extracellular matrix vesicles were scattered between the forming cells and the calcifying fronts. Some of the vesicles contained electron-dense material and in others, apatite crystals were detected. Matrix vesicles could not be identified in normal, mature calcifying dentin matrix. In view of the present observations and studies on surgical manipulations in articular cartilage, it is concluded that matrix vesicle calcification may result from alterations in the metabolic state of mesenchymal tissues. These changes can be induced surgically or chemically.

Animals↗
PubMed2002

Partial rescue of the Hyp phenotype by osteoblast-targeted PHEX (phosphate-regulating gene with homologies to endopeptidases on the X chromosome) expression.

Inactivating mutations and/or deletions of PHEX/Phex (phosphate-regulating gene with homologies to endopeptidases on the X chromosome) are responsible for X-linked hypophosphatemic rickets in humans and in the murine homolog Hyp. The predominant osteoblastic expression of Phex has implicated a primary metabolic osteoblast defect in the pathophysiology of this disorder. By targeting PHEX expression to osteoblasts in the Hyp genetic background, we aimed to correct the corresponding biochemical and morphological abnormalities and obtain information on their pathogenetic mechanism. When transgene Phex expression, driven by a mouse pro-alpha1(I) collagen gene promoter, was crossed into the Hyp background, it improved the defective mineralization of bone and teeth but failed to correct the hypophosphatemia and altered vitamin D metabolism associated with the disorder. Ex vivo bone marrow cultures confirmed the amelioration in the Hyp-associated matrix mineralization defect after Phex expression. These findings suggest that while the Hyp bone and teeth abnormalities partially correct after PHEX gene transfer, additional factors and/or sites of PHEX expression are likely critical for the elaboration of the appropriate molecular signals that alter renal phosphate handling and vitamin D metabolism in this disorder.

Alkaline Phosphatase↗
PubMed1996

Extracellular processing of bone and dentin proteins in matrix mineralization.

There are two steps in the process of matrix-mediated bone and dentin mineralization. First, as in other soft tissues, osteoblasts/odontoblasts synthesize collagenous matrices and second, mineral deposits in these matrices at a location distant from the cells that synthesized the matrices. We suggest a sequence of events that lead the matrix to mineralization: the phosphoproteins of bone and dentin are posttranslationally processed by limited proteolysis, then they are extracellularly processed into a more phosphorylated species that, we believe, facilitates mineralization. Our in situ phosphorylation experiments done with [gamma-32P] GTP suggest the existence of extracellular phosphorylation by a casein kinase II (CKII)-like enzyme, the enzyme known to phosphorylate most of the phosphate residues in dentin phosphophoryn and bone sialoproteins (osteopontin and BSP II).

Adenosine Triphosphatases↗
PubMed1993

Relationships between mandibular canine calcification stages and skeletal maturity.

Hand wrist radiographs and dental panoramic radiographs of 200 boys and 215 girls were assessed to determine the relationship between the developmental stages of the mandibular canine and skeletal maturity indicators of the pubertal growth spurt. Chi-square and Kendall's tau statistics demonstrated significant (P < 0.001) relationships between skeletal maturity indicators. Associations between canine development and skeletal maturity ranged from 0.53 to 0.85. Most children having attained canine stage G showed the presence of the adductor sesamoid (81%), capping of the diaphysis of the third middle phalanx (77%), and capping of the fifth proximal phalanx (87%). Growth reference data for American children suggest that stage G occurred approximately 0.4 years and 1.3 years before peak height velocity for girls and boys, respectively. It is indicated that canine calcification could serve as a useful tool for evaluating childrens' skeletal maturation and, by association, somatic maturity.

Adolescent↗
PubMed2004

Accelerated bone formation and increased osteoblast number contribute to the abnormal tooth germ development in parathyroid hormone-related protein knockout mice.

Our previous study showed that tooth germs at late embryonic stage [later than embryonic day 17.5 (E17.5)] and neonatal homozygous parathyroid hormone-related protein (PTHrP)-knockout mice are compressed or penetrated by the surrounding alveolar bone tissue. In vivo and in vitro studies have shown that the development of the tooth germ proper is not disturbed, but insufficient alveolar bone resorption, due to the decreased number and hypofunction of osteoclasts, is the main cause of this abnormality. In addition to the insufficient alveolar bone resorption, progressive bone formation toward tooth germs was observed in homozygous mice, suggesting that accelerated bone formation also contributes to this abnormality. To further investigate this, homozygous mice at E14.0 and E15.5, when alveolar bone is forming, were used for histochemical and bone histomorphometric analyses. In contrast to the late embryonic stage, the alveolar bone did not yet compress developing tooth germs in homozygous mice on E14.0, but a larger amount of bone tissue was seen compared to wild-type littermates. Histomorphometric analysis of bone at E14.0 revealed that the osteoblast numbers and surfaces in the mandibles and in the bone collar of femora of homozygous mice were significantly higher than those of wild-type mice. However, unlike our previous study showing the osteoclast surface on E18.5 in homozygous mice to be significantly lower than that of wild-type mice, this study at E14.0 showed no significant difference between the two genotypes. To evaluate the amount of calcification around tooth germs, 3D images of mandibles were reconstructed from the calcein-labeled sections of the wild-type and mutant mice. Labeling was performed at E14.0, and the mice were sacrificed 1 h after the calcein injection to minimize the effect of bone resorption. Comparison of the 3D images revealed that the labeled surface was larger around developing tooth germs in homozygous mouse than in wild-type mouse. On day E15.5, osteoblasts approached the enamel organ of homozygous mice but this was not observed in wild-type mice. In this study, we report a systemic increase in osteoblast number and accelerated bone formation in homozygous PTHrP-knockout mice, both of which contribute to the abnormal tooth development.

Acid Phosphatase↗
PubMed1994

Morphological studies of hypomineralized enamel of rat pups on calcium-deficient diet, and of its changes after return to normal diet.

BACKGROUND: Micro-hardness investigations have shown that rat pups nursed by mothers on a low calcium diet and weaned with the maternal calcium-deficient diet develop hypomineralized enamel. The inorganic and organic components of this enamel, their relationships, and their changes after return to normal diet have been studied by light and electron microscopy. METHODS: The maturation zone of incisor enamel has been studied in: (1) rats nursed for 20 days by mothers on a low calcium diet and weaned for 30 days with the same diet (E1 enamel); (2) rats that after the calcium-deficient diet were fed normal diet for 10 days (E2 enamel); and (3) rats nursed for 20 days by mothers on a normal diet and weaned for 30 days with a normal diet (controls). RESULTS: The results showed that E1 enamel was hypomineralized, as noted by its Azure II-Methylene blue stainability in undecalcified sections, its light staining with the von Kossa method, and its ultrastructure. E1 crystallites, although present throughout the whole enamel, were thinner than those of E2 enamel, which were similar to those of controls. E1 interrod crystallites were thicker in the intermediate than in the dentinal zone and were thicker than rod crystallites. Organic matrix was present throughout the whole E1 enamel. Its organic components (crystal ghosts) had the same shape, arrangement, and organization as those of inorganic crystallites. Crystal ghosts were greatly reduced in E2 enamel and in controls. CONCLUSIONS: The results lead to the conclusions that: (1) E1 enamel is hypomineralized, and its degree of calcification is restored by return to a normal calcium diet; (2) intra- and interprismatic calcification occurs in a different way; (3) crystallite thickness is initially greater in dentinal than in the superficial zone and is reversed as crystallite growth is completed; and (4) loss of enamel proteins is necessary for completion of crystallite growth and not for crystallite formation.

Animal Nutritional Physiological Phenomena↗
PubMed2002

[The study of calcification of autogenous bone marrow stem cell transplantation on alveolar bone defect in dogs].

OBJECTIVE: To evaluate the effect of calcification of autogenous bone marrow stem cell transplantation in periodontal tissue regeneration. METHODS: Bone marrow stem cells derived from the same dog were cultured with alpha-MEM. 1 x 10(7) cells of first passage were allowed to attach to the collagen membrane for 24 hours. The membrane-cells were transplanted into periodontal defect in the same dog. Then the defects were covered with e-pTFE membranes. The defects covered only with e-pTFE without membrane-cells were served as control. Eighteen teeth of 6 dogs for every group were studied. The dogs were sacrificed after 6 weeks. RESULTS: The results showed that new bone formation in test group was significantly higher than that of control group. The calcification of new bone in test group was better than control group. CONCLUSIONS: The results suggested that autogenous bone marrow stem cell transplantation with guided tissue regeneration technique could enhance periodontal tissue regeneration and could form new bone tissue fast and could shorten times of periodontal tissue regeneration in dogs.

Alveolar Bone Loss↗
PubMed2001

The in vitro and in vivo influence of 4-META/MMA-TBB resin components on dental pulp tissues.

The purpose of this study was to qualitate the penetration of the major components of 4-META/MMA-TBB adhesive resin (4-META resin) and to characterize their influence on the in vitro and in vivo wound healing of dental pulp tissues. Fresh 4-META resin was applied to rabbit mesentery; its components penetrated the mesentery to form three of layers, depending on the amounts of monomer components in the tissue. The superficial layer was a soft-tissue hybrid layer (STHL), the intermediate layer contained small particles of polymerized 4-META resin, while the deepest layer contained unpolymerized monomer components including MMA and butanol, which were detected by gas chromatography (GC). To characterize the in vivo effects of the deepest layer, we immersed the pulp tissue in MMA or in 5% 4-META/MMA and autotransplanted it to placement beneath a rabbit kidney capsule. The MMA-immersed pulp was positive for osteocalcin and presented osteodentin formation at 7 days, as did the untreated control pulp tissue. In contrast, the 5% 4-META/MMA-immersed pulp collapsed into the cell-deficient fibrous connective tissue, with slight calcification by 7 days and less osteodentin formation at 14 days. Analysis of these data suggests that MMA does not inhibit osteogenic activity of pulp tissue, while 5% 4-META/MMA does inhibit osteogenic activity to some extent.

Acrylic Resins↗