The specificity of the 3H-proline incorporation test as a measure of bone matrix formation.
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In a co-culture system of mouse spleen cells and osteoblastic cells, we have demonstrated that a suitable microenvironment must be provided by osteoblastic cells in order for osteoclast-like multinucleated cell (MNC) formation. Using this co-culture system, we examined the pathogenetic mechanism underlying the lack of bone resorption in osteosclerotic oc/oc mice. Numerous tartrate-resistant acid phosphatase (TRAP, an osteoclast marker enzyme)-positive MNCs were formed in response to 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3] both in co-cultures of oc/oc spleen cells and normal osteoblastic cells and in those of normal spleen cells and oc/oc osteoblastic cells. TRAP-positive MNCs derived from normal spleen cells tended to spread out on culture dishes, whereas those from oc/oc spleen cells remained as small, compact MNCs. When TRAP-positive MNCs enriched from co-cultures of normal spleen cells and oc/oc osteoblastic cells were cultured on dentine slices, they formed numerous resorption pits with ruffled borders and clear zones. In contrast, none of the TRAP-positive MNCs derived from oc/oc spleen cells formed either ruffled borders or resorption pits. These results indicate that the lack of bone resorption in oc/oc mice is due to a defect in osteoclast progenitors rather than the local microenvironment provided by osteoblastic cells.
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Osteopetrosis in mammals results from a congenital reduction in bone resorption. Calvarial organ cultures were used to measure bone resorption in osteosclerotic (oc/oc) mice and their normal littermates. Measurements of cell-mediated resorption indicate that baseline isotope release by mutant calvariae was only 57% of that observed in normal littermates and isotope release by mutant bone in the presence of parathyroid hormone (PTH) was only 60% of that in normal controls. However, the response of oc calvariae to PTH was not different from normal bone when considered with respect to baseline resorption. These data indicate that bone resorption in oc mice is reduced in both its basal level and in response to PTH and suggest that oc mice are unable to establish normal baseline resorption which may in turn compromise their responsiveness to PTH.
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Patients with teeth showing all of the clinical, radiographic, and histologic features of radicular dentine dysplasia (type I) have been found to have dense sclerotic bone and skeletal anomalies of the wrists and hand bones. The association of these defects of teeth and bone was found to be transmitted as an autosomal dominant trait over four generations. Review of theliterature failed to disclose a previous description of this disorder.
A case of pyknodysostosis in a 32-year-old woman has been reported. The patient presented typical skeletal changes, separated cranial sutures, open fontanelles, partial aplasia of the terminal phalanges of the fingers and toes, and brachyphalanges. The oral findings included lesions resembling periapical cementoma, hypoplasia of the maxilla and mandible, crowding of teeth, and a median raphe.
Forty-nine roots of thirty-six teeth with the diagnosis of condensing osteitis were followed up by means of radiographs and patient files after endodontic treatment. The mean observation period was 4.3 years. Prior to endodontic treatment the periodontal membrane was widened on thirty-eight roots but on follow-up only on twelve. The periapical condensing osteitis showed total regression on thirty-six of the forty-nine roots. No condensing osteitis showed progress. The results show rebuilding of bone structures to normal appearance after endodontic treatment of periapical condensing osteitis.
Erdheim-Chester disease is a rare histiocytosis also known as lipoid granulomatosis. Oral findings have not been reported previously to our knowledge. This case report documents evidence of oral sequelae of Erdheim-Chester disease. A patient whose course was followed for 10 years at the National Institutes of Health had premature alveolar bone resorption. He underwent full-mouth extraction at age 29 years because of severe periodontitis. Histopathologic evidence of Erdheim-Chester disease was demonstrated in the periodontal soft tissues. In the ensuring years, accelerated resorption of the residual ridges precluded the use of conventional dentures. We recommend early preventive dental management for patients with Erdheim-Chester disease.
A high frequency of remodeling changes was demonstrated radiographically in a series of 200 female patients with asymptomatic temporomandibular joints. Fewer than 10% of joints were completely radiologically "normal". Generally, there was an increasing incidence of changes with increasing age and for edentulous patients, but these relationships were by no means direct or mutually exclusive.
The purpose of this study was to evaluate the long-term clinical and radiologic effects of a temporary silicone implant after diskectomy of the temporomandibular joint. Forty-three temporomandibular joints in 43 patients with painful disk displacement underwent a diskectomy. A sheet of medical-grade silicone was temporarily placed in 22 patients; 21 patients did not receive an implant. The patients were clinically and radiologically examined 5 years after surgery. On the basis of symptoms and jaw function, they were classified as having good (30 patients), acceptable (8 patients), and bad (5 patients) results. All the patients with bad results and five of the eight patients with acceptable results had received implants. Erosive changes of the condyle or fossa were seen radiographically at follow-up in eight patients, each of whom had received an implant. No positive clinical or radiologic effects of the implants could be identified. The use of a temporary silicone implant after diskectomy of the temporomandibular joint in patients with internal derangement should be seriously questioned.
The purpose of this study was to provide an objective analysis of the radiographic characteristics of histiocytosis X as it affects the jaws. The original radiographs of 29 cases were reviewed independently and objectively by three observers. The results suggest that seven characteristics, either alone or in combination, are useful in the identification of histiocytosis X. These include the appearance of solitary "intraosseous" lesions, the multiplicity of "alveolar bone" lesions, the "scooped-out" effect in the alveolar process, the well-defined periphery, sclerosis in the alveolar bone lesions, periosteal new bone formation, and slight root resorption.
One hundred thirty-one arthrographic examinations of temporomandibular joints were performed on 119 patients. The relationships between clinical symptoms, tomographic findings, and soft-tissue perforation were examined. Perforations of the articular disk or posterior attachment were revealed in 58 joints. Joints with crepitation showed a high frequency of perforation (20 of 22). Pain in the joint area and limitation of opening correlated to disk reduction. Perforations were observed in 12 of 21 joints with continuous pain. Osseous changes were detected in 89 joints. Joints with abnormal radiodensity (erosion, sclerosis) combined with abnormal shape (pocket erosion, osteophyte formation, deformity) showed a high frequency of perforation (41 of 45), which corresponded to 84% in this study. In those cases with osseous change or crepitation, positive predictive values of perforation were both 91%. These types of osseous change and their clinical significance might predict soft-tissue perforation with high accuracy before an arthrogram is performed.
Masticatory inhibitory mechanisms were studied in 10 patients treated for diffuse sclerosing osteomyelitis of the mandible. Their masseter inhibitory reflex responses were provoked electrically by mental nerve stimulation during maximal clenching of the teeth. The masseter inhibitory reflex was normal in two patients and significantly abnormal in eight patients. The two patients with a normal masseter inhibitory reflex were free of complaints, whereas, of the eight patients with an abnormal masseter inhibitory reflex, two were free of complaints and six had moderate to severe symptoms. In three patients, spasms and involuntary bursts of electromyographic activity were found. The abnormal masseter inhibitory reflex consisted of a loss of early and late components in four patients or a loss of the late component with a normal early one in four patients. These findings seem to support the hypothesis that diffuse sclerosing osteomyelitis of the mandible is a chronic tendoperiostitis caused by muscle overuse. It is suggested that this overuse is caused by central hyperexcitability of trigeminal motoneurons.