Action of trace elements in the mineralisation of hard tissues.
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Tooth luxations are relatively common. In case of concussion or subluxation the tooth is not displaced. The treatment will consist of relief of the tooth. Most frequent complications are pulp necrosis and obliteration of pulpal tissues. In case of extrusive luxation pulpal tissues and the periodontal ligament are injured. When tooth mobility is increased flexible splinting should be considered. Endodontic treatment is necessary after extrusive luxation of a tooth with completed root formation. Teeth with open apex often show pulpal obliteration after extensive luxation. Lateral luxation is more complex than extrusive luxation since the alveolar bone is also damaged. Repositioning and splinting of the tooth are necessary. When the apical foramen in closed, endodontic treatment will be necessary. Teeth with incomplete root formation will develop pulp obliteration. Following lateral luxation, external root resorption and loss of marginal bone are not infrequent. Intrusive luxation is the type of trauma with most unfavorable prognosis. All intruded teeth will become necrotic and external root resorption and marginal bone loss are frequent. There is no consensus regarding the therapeutic approach. Orthodontic extrusion or surgical mobilisation are possible options. In case of avulsion, both the pulpal tissues and the periodontal ligament are disrupted. Preservation of the vitality of the periodontal ligament covering the root will determine the prognosis of the reimplanted tooth. Therefore the tooth will be repositioned as soon as possible. When this is not possible, milk or a specific solution are most appropriate for tooth conservation. When the reimplanted tooth has complete root formation, devitalization will be performed one week after after repositioning. In case of a tooth with open apex revascularisation can be awaited. Healing of the periodontal ligament will determine prognosis. When a normal ligament is obtained during healing or when surface resorption is obtained, the tooth can be preserved for a long period. When progressive replacement resorption (ankylosis) develops, most teeth can remain in position for about 10 years. When inflammatory resorption develops, the tooth will be lost within a short time.
AIM: The purpose of this histological study was to examine teeth with hyperplastic pulpitis caused by trauma or caries. SUMMARY: The pulp tissue of one young permanent incisor with a complicated crown-root fracture and a hyperplastic pulpitis, which had been contaminated with oral microflora for 40 days, and pulp polyps from four permanent first molars whose crowns were destroyed by extensive caries were prepared for standard histological examination. Histologically, normal pulp tissue organization was observed in the tooth with a complicated crown-root fracture in the cervical radicular region. Irregular calcification was seen in the coronal and radicular portion of the pulp in the four carious teeth with pulp polyps. Radicular pulp tissue in the middle and apical third of root canals beneath irregular calcification showed intensive fibrosis but was free from inflammatory cells. KEY LEARNING POINTS: Hyperplastic pulpitis is a type of irreversible chronic open pulpitis. Young permanent teeth with hyperplastic pulpitis caused by trauma or caries have a great inherent defensive capacity to heal.
Under general anaesthesia, 35-day-old female rats were ovariectomized and the right maxillary molar teeth removed. Dynamic measures of alveolar bone formation were determined at 10 days after surgery, using the fluorochrome labelling technique, and compared with control animals. Ovariectomy significantly increased buccal resorption and palatal bone formation. In a second experiment, ovariectomized rats had the right maxillary molar teeth extracted and were killed at either 5 or 14 days after surgery. The mean mineralizing surface of the alveolar bone (percentage of surfaces occupied by a double fluorescent label) was significantly lower in rats killed at either 5 or 10 days than at 14 days after ovariectomy and tooth extraction. The mean appositional rate was significantly greater at 5 days after ovariectomy and tooth extraction than at 10 or 14 days. Oestrogen deficiency can therefore affect alveolar bone turnover following tooth extraction.
In order to elucidate the mechanism of adhesion between the gingiva and the tooth, detailed comparative ultrastructural studies of the dentogingival border were done in the monkey and shark. The tissues were prepared with or without demineralization for the ultrastructural observations. At the border, the internal basement membrane, which is firmly bound to the junctional epithelium through hemidesmosomes, was specialized differently in these species. In the monkey, the lamina densa was closely associated at its enamel side with an additional layer which had characteristics of the lamina densa and was referred to as the supplementary lamina densa. In the shark, the lamina densa showed a unique, hemidesmosome-related specialization in the form of the intermittent occurrence of bulges along its surface facing the epithelium. In nondemineralized tissues a part of the basement membrane, that is, the supplementary lamina densa (monkey) and the main lamina densa but not bulges (shark), was preferentially mineralized. The mineral deposit was continuous with that in the enamel and enameloid/dentine, thus constituting an advancing edge of mineralization. The network arrangement of the mineral crystals in the monkey basement membrane resembled the pattern of the cord network of the basement membrane, suggesting the presence of a delicate mutual basement membrane-mineral interaction. Thus, the organic phase and the mineral phase are allowed to make contact at this mineralized area of the basement membrane and firmly bind to one another. Therefore, strong gingiva-tooth adhesion is established by partial mineralization of the internal basement membrane, in a way similar to that found in the previously reported association of maturation stage ameloblasts with the enamel.
Alveolar bone of erupting teeth was studied in order to define the types of calcified tissues deposited as well as the rate of tooth growth. The third (P3) and fourth (P4) mandibular premolars of 30 dogs aged 12-24 weeks were analyzed by microradiography and microscopy in fluorescent and ordinary light. The bone plate separating P3 and P4 from the mandibular canal presented a complex arrangement of lamellar and woven bone, and even of chondroid tissue. During the pre-eruptive phase, this plate shifted towards the base of the mandible by means of selective resorption and apposition activities. As soon as the furcation was formed, bone apposition appeared on the alveolar side and became the main activity under P3 at the outset of eruption. Under the roots of P4 it occurred 4 weeks later. Dynamic morphometry in fluorescence microscopy showed that eruption progressed faster than the radicular growth. The formation of interradicular bone underwent the same acceleration as the eruption. However, though the tissues were formed at a high rate, it cannot be inferred therefrom that they are responsible for tooth shifting. They might just fill the space left by the erupting tooth.
Three clinical cases of odontoma were detected in 2 children and 1 adolescent. The tumors were surgically removed. Clinical suspicion was based on facial deformity in one of the cases and on the absence of permanent tooth eruption in the other two. Radiographic evidence of odontoma was confirmed through histological study.
The degenerating tissues found in rat periodontal ligaments during tooth movement were examined morphologically, histochemically, and elementally, with decalcified and unfixed, undecalcified frozen sections. There were two types of degenerating tissues found in the compressed periodontal ligaments: One (type A tissue) was stained differently from collagen and the other (type B tissue) showed the same color as collagen. Type A tissue also showed the deposition of fibrin in Martius scalet blue and Weigert stain. The electron micrograph also showed the deposition of fibrin in type A tissue. No collagen fibers with typical bandings were seen in either tissue. The digestion experiment showed that type A tissue was digested by trypsin but not type B, whereas most of type B tissue was digested by collagenase but not type A. The backscattered electron image by scanning electron microscopy of type A tissue of the unfixed undecalcified frozen sections showed the presence of many small pieces. The elemental analysis of the pieces showed high peaks of phosphorous and calcium. These results indicate that collagen degradation, fibrin deposition, and calcification occurred in the degenerating tissues, especially in type A tissue during the experimental tooth movement.
A ten-year-old boy, who had the typical dental findings of dysosteosclerosis such as yellowish, hypoplastic teeth, retarded eruption, which upon eruption, decayed rapidly, is presented. To date this is the first known case reported with a congenital absence of the first permanent molars. Furthermore, SEM evaluation of the enamel and dentin was performed on a tooth from a patient with dysosteosclerosis for the first time. These studies showed weak ultrastructural compositions due to irregular calcification.
A 36-year-old woman was examined and treated for a rare odontogenic tumor in the mandible, the calcifying epithelial odontogenic tumor (CEOT), also known as the Pindborg tumor. The tumor extended from the left mandibular molar region to the right premolar area and had almost completely destroyed the bone in the anterior mandibular region. An orthopantomogram showed a multiloculated radiolucent lesion, with an unerupted tooth in the center surrounded by a radiopaque area. In addition, finely granular calcification was visible here and there in the tumor area. In the histologic examination the tumor tissue could be identified as calcifying epithelial odontogenic tumor. Under electron microscopy the fibrillar structure at the basal cell level suggested the presence of amyloid. The tumor was removed by enucleation with a collar of surrounding tissue. No signs of recurrence have been noted at follow-up examinations.
An interesting case is reported, of calcification of the dental papilla. As yet, little is known about this asymptomatic calcification, which constitutes a rare radiographic finding, deforming the root of a vital tooth, generally a lower premolar or canine.
Although the adenomatoid odontogenic tumor (AOT) is categorized as an odontogenic epithelial tumor with odontogenic ectomesenchyme, AOT with induction of true tubular dentin with or without concomitant formation of enamel is exceedingly rare. This paper reports a case of AOT showing evidence of extensive induction of tubular dentin, but without concomitant formation of enamel. The patient was a 20-year-old female with a rather well-circumscribed intraosseous lesion of the maxillary incisor-premolar area without an embedded tooth. Histologically, extensive induction of a dysplastic form of tubular dentin with globular calcification was evident, in addition to the characteristic histological features of AOT. The present case lends support to the categorization of AOT as an odontogenic tumor consisting of a disorderly mixture of odontogenic epithelium and odontogenic ectomesenchyme with or without dental hard tissue formation.
References in the endodontic literature specifically warn that orthodontic treatment may initiate the formation of secondary dentin deposition within a tooth to the extent of obstructing the entire root canal. Comparison of forty-six orthodontically treated patients with a control group of age- and sex-matched patients who had not undergone orthodontic treatment revealed two orthodontically treated patients with a total of three teeth that showed evidence of canal calcification. Although this incidence is not statistically significant, the clinical significance of canal calcification in the orthodontic population is discussed.
Two renal dialysis patients with oral manifestations of oxalosis had undecalcified sections of iliac and alveolar bone and teeth examined histologically in an attempt to explain the development of tooth mobility and tooth loss. Osteomalacia was detected in all bone specimens and attributed to aluminum toxicity after the histochemical localization of aluminum at the calcification front between osteoid and calcified matrix. Aluminum was also detected histochemically in the cementum of teeth. Calcium oxalate crystals were present in bone marrow, teeth, and gingiva. It is proposed that tooth mobility and tooth loss in oxalosis result from the combined effects of osteomalacia and oxalate crystal deposition within the periodontium. To prevent avoidable tooth loss it is suggested that patients with oxalosis who develop tooth mobility should have aluminum toxicity and osteomalacia excluded as causal factors.
OBJECTIVE: To evaluate the role of matrix vesicles (MVs) during the development of mineralizing tissues. METHODS: The ultrastructure of MVs of tooth germ, calvarial bone and mandibular bone were observed by transmission electron microscopy in fetal Wistar rat. RESULTS: (1) The MVs were formed by osteoblast of the secret type, dentinoblast and process; (2) There was a mature process of the MVs in the extracellular matrix. The appearance of the hydroxyapatite (HAP) was a major mature feature; (3) HAP formed initially in the MVs entered into collage matrix and eventually mineralized; (4) The shifting sign of HAP from MVs to the surface of collage fibril was observed. CONCLUSIONS: The MVs played an important role in the biomineralization, but the special arrange pattern of mature collage fiber provided a suitable environment and a model to the growth of HAP for further mineralization.
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Light microscopy, microradiography, SEM and TEM of 4 tooth follicles in a 12-year-old caucasian girl presenting regional odontodysplasia showed widespread globular dentin, calcifications located in the enlarged pulp chambers, hypoplastic and hypomineralized enamel. Hypomineralized strands were sandwiched between two normal enamel layers, which indicates that amelogenesis, interrupted for a while, has once more become established. The enamel surface was covered with calcoglobules. Numerous rounded calcifications were scattered within the dental follicles. Some of these occurred in microfibrils (possibly oxytalan fibers), distinct from collagen fibers. Calcification of the sheath surrounding epithelial rests was a conspicuous feature. The fibroblasts in contact with calcifications developed numerous cytoplasmic extensions, which suggests that they may have assumed a phagocytosis behaviour.