Bleaching of root canal treated teeth and cervical external resorption: review of the literature.
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The aim of this study was to determine, the effect of physiological root resorption on the histological structure of healthy primary tooth pulp. Fourteen canine teeth, which needed to be extracted for orthodontic purposes and in which resorption had just begun (1st group, resorption did not exceed 1/3 of root length) or was in advanced resorption stage (2nd group, resorption was between 1/2 and 2/3 of root length), were used for this study. After the extraction of the teeth, they were prepared for histological examination. Then the samples were examined using light microscopy. The result no difference was found which could be detected by polarized light microscope that was related to physiological resorption and histological structure of primary teeth pulp.
A maxillary incisor that had been replanted immediately after avulsion 49 years previously was evaluated histologically after extraction. The histological evaluation revealed resorption of the apical root surface, depositions in cement with different phases and mineral density, and histological changes in the periodontal ligament.
The purpose of the present investigation was to describe the formation, maturation and eruption of the dentition, including supernumerary teeth in a sample of patients with cleidocranial dysplasia. The dentition was evaluated from orthopantomograms, intraoral radiographs, cephalometric films, surgically removed teeth and intraoral photographs in 19 patients (9 men, 10 women), aged 3.5 to 34 years. Formation of primary teeth was normal, whereas all patients but one had supernumerary permanent teeth. Frequency of supernumerary teeth ranged from 22% in the maxillary incisor region to 5% in the molar regions. Supernumerary teeth were formed lingually and occlusally to the normal teeth. Maturation of the primary dentition was normal, while permanent teeth were delayed from 1 to 4 yr. Supernumerary teeth were delayed about 4 years in relation to normal permanent teeth. Eruption of primary teeth was normal, whereas all patients had severe eruption problems of permanent teeth. It was hypothesized that the dental lamina for both primary and permanent dentition is normal, but does not resolve completely and therefore may form supernumerary teeth. Abnormalities of tooth morphology is related to inadequate space and arrested eruption. Delayed or arrested eruption is probably caused by diminished resorption of bone and of primary teeth and to the presence of multiple supernumerary teeth.
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The protective role of cementum against root resorption is discussed in relation to buried teeth, orthodontic treatment, replantation and periodontal disease. The essential feature seems to be a layer of partially calcified precementum or vital cementoblasts. Root resorption close to the epithelial attachment, although not common, is probably the result of death of cementoblasts caused by irritants from bacterial plaque, and the presence of severe of prolonged inflammation. Cementum exposed in the pocket can be affected in different ways by these irritants, and rendered unacceptable for re-attachment to periodontal tissue. Successful re-attachment procedures involve either the removal of the affected cementum or its treatment with agents partially to decalcify such as acids, or detoxify by phenol for example. Examples of treatment embodying some of these principles are illustrated by two case histories of localised gingival recession and one of intra-bony pocketing associated with an acute lateral periodontal abscess. In this case a follow-up radiograph taken 16 years later is presented as evidence of the permanence of repair which can be achieved. Root resorption which often follows the use of fresh autogenous bone from the ilium is then discussed and the conclusion reached that the vital cells in the transplant discourage the migration of cementoblasts from the adjacent periodontium. The cementum and dentine thus remain unprotected and susceptible to resorption.
This study demonstrated the simultaneous expression of cathepsin K (CK) mRNA by in situ hybridization and CK protein by immunoelectron microscopy in odontoclasts in mouse maxillae after experimental tooth movement. On the pressure side (the area under pressure during tooth movement), CK mRNA was detected in odontoclasts in resorption lacunae in the tooth root, in osteoclasts in bone resorption lacuane, and in fibroblasts in the periodontal ligament. Using electron microscopy, CK protein was detected at the apex of odontoclasts, intracellularly in vesicles and granules, and extracellularly in irregularly shaped vacuoles (extracellular spaces), on the plasma membrane of the ruffled border, and on and between typical striated type I collagen fibrils in the lacunae. These vesicles and granules appeared to fuse with irregular vacuoles containing CK-positive fragmented fibril-like structures close to the ruffled border. In the basolateral portion of odontoclasts, small amounts of CK-positive rough endoplasmic reticulum (ER) were found. CK-positive intracellular vacuoles (not extracellular spaces) also appeared to fuse with the vesicles and granules. However, these fused organelles rarely contained fragmented fibril-like structures. They are probably endolysosomes. The distribution of CK in odontoclasts was similar to that previously seen in osteoclasts. Furthermore, CK-positive fibril-like structures were found in the vacuoles of fibroblasts. These results indicated that during tooth movement CK is synthesized in odontoclasts on the pressure side and secreted into the tooth resorption lacunae. Therefore, CK may take part in the degradation of the dentin matrix (type I collagen fibrils and non-collagenous protein) of the tooth root, and in the subsequent intracellular degradation of endocytosed fragmented fibril-like structures in endolysosomes.
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A host-derived neutrophil-activating cytokine interleukin-8 (IL-8) is secreted mainly by monocytes and is considered to be important in regulating alveolar bone resorption during tooth movement. The aim of this study was to evaluate the levels of IL-8 during mechanical forces on periodontal tissues at different stages of orthodontic therapy. Ten canine teeth of patients having different Angle classifications were selected for the study. After the premolars were extracted, the maxillary/mandibular canines were tipped distally. Gingival crevicular fluid was sampled from mesial and distal gingival crevices of each canine separately at baseline and one hour, 24 hours, six days, 10 days, and 30 days after the application of the force. An enzyme-linked immunosorbent assay for quantitative detection of IL-8 was used. Although there was an increase in the concentration of IL-8 at tension (mesial) sites after one hour, 24 hours, six days, and 10 days, a decrease was observed at 30 days. Pressure (distal) sites did not demonstrate such an increase at any period except at 10 days. However, the concentration of IL-8 at both sites showed a similar decrease and approached each other at day 30. We concluded that local host response toward the orthodontic forces might lead an increase in IL-8 and neutrophil accumulation, and this may be one of the triggers for bone remodeling processes.
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