No abstract

The effect of interleukin-1 beta, the major component of osteoclast-activating factor (OAF), on bone formation by fetal rat osteoblast-rich cells was investigated. An in vitro culture system developed by Ecarot-Charrier et al. (1983) and Bellows et al. (1986) was utilized in which osteoblasts form mineralized nodules which closely resemble woven bone. Continuous exposure of cultures to homogenous IL-1 beta resulted in potent inhibition of mineralized nodule formation, which was half maximal at 0.1 U/ml (7.5 X 10(-13) M). Bone formation may thus be considerably more sensitive to IL-1 beta than is bone resorption (half maximal at 3.8 X 10(-11) M). Inhibition of bone formation occurred when cultures were exposed to IL-1 beta at both early and late time periods and was unaffected by the presence of indomethacin or by the osteoclast inhibitors calcitonin and gamma-interferon. Instead, IL-1 beta exerted multiple inhibitory effects on osteoblast functions, including inhibition of collagen and noncollagen protein synthesis, alkaline phosphatase expression, and cell replication. On a dose response basis, the inhibition of protein synthesis correlated most closely with inhibition of bone formation. IL-1 beta is clearly inhibitory rather than stimulatory for bone formation as assessed in this system and is therefore unlikely to function as a coupling factor linking the processes of bone resorption and bone formation.

No abstract

Seventy‐six weanling gnotobiotic rats of the Sprague‐Dawley strain were monoinfected in groups with Actlnomyces naeslundii, Actinomyces viscosus or Streptococcus mutans. The animals were killed at intervals up to 84 days and the maxillae and mandibles examined histologically. Periodontal disease, as evidenced by the presence of plaque, migration of the epithelial attachment and regression of the alveolar bone was sometimes evident after 28 days and in all cases extreme by 84 days. No organisms were seen in the gingiva and inflammatory changes were slight. Periodontal disease was most marked between the first and second maxillary molars, the mandibular gingiva, apart from the presence of plaque, being normal over the experimental period. Bone loss was gauged by labelling the bone with 3H proline, and osteoclasts were detected by the acid phosphatase technique. In another experiment, 44 conventional weanling cream hamsters were superinfected with A. naeslundii. Periodontal disease developed more slowly than in the gnotobiotic rats, usually taking about 160 days to be severe. In both experiments the pathological changes were similar. The gnotobiotic rats developed periodontal disease over the same time sequence with all three organisms. Bone loss was not accompanied by the presence of osteoclasts and seemed, in this model, to be more due to a gradual cessation of bone formation than to active resorption. If in addition bone resorption did occur, it was brought about by a mechanism at present undescribed.

Since compact bone is demonstrably anisotropic and inhomogeneous, the measured quantities yield a plesio-velocity rather than a true sonic velocity, which makes it difficult to compare velocity measurements among several bone samples. Distribution of the plesio-velocity for 11 pairs of 2 mm thick specimens from a single mature bovine compact bone sample using 100-ns well-damped sonic pulses emitted by a 10-mHz transducer show that anisotropy exists in both axial and transverse directions and must be associated with the local structure and composition. Changes in the same specimens when wet, dry, and rehydrated show an increase in velocity and anisotropy of the dry over the wet state. The plesio-velocity is greater in the axial direction, along the bone axis, than in the transverse plane. The change in plesio-velocity from wet to dry bone is greatest along the bone axis and least in the transverse plane. Changes in dimension, when the bone specimens were dried, show the bone sample to be anisotropic in this parameter also, but in the reverse order from that for the plesio-velocity. Shrinkage is least along the osteons and a maximum in the transverse plane.

We examined the effects of phosphoric acid, the most common enamel etchant in composite resin therapy, on dentine collagen. Dentine collagen pretreated with 7M phosphoric acid was shown to be more susceptible to trypsin digestion than untreated collagen. This susceptibility increased with increasing duration of exposure to the acid. The results indicate that phosphoric acid induces a conformational change in dentine collagen (denaturation or perturbation) similar to that observed with 0.39 M HCl, which has a similar pH value (0.65). However, phosphoric acid-pretreated dentine collagen, when treated with tannic acid for 2 h, became as resistant to tryptic digestion as intact dentine collagen. The present results suggest that tannic acid may work as a dentine conditioner in composite resin therapy, in view of the fact that phosphoric acid etchant is applied, either deliberately or inadvertently, to dentine, and would thus induce denaturation or perturbation of collagen.

The density of a bovine cortical bone matrix sample was found in water, several ethanol-water solutions, and in dried state. Previously the density of the same mineralized bone was found fresh and when desiccated. The volume in each state was estimated from the dimensional changes axially, tangentially, and radially. Confirmation was found by determining the density of dried specimens upon immersion in xylene. The amount of imbibed xylene provided an estimate of the free pore volume in the dried matrix. The volume fraction of the solid constituent, S, in the wet matrix was found to be 0.57, from which the density of S in various solutions was calculated. Density of wet matrix in 0.15 M saline: 1.180 g/cc; for dried matrix, 1.246 g/cc. Density of wet S in saline: 1.33 g/cc; for dried S, 1.42 g/cc, which matches published values for collagen molecules. Dimensional changes between wet and dried state of matrix match published values for artificially cross-linked rat tail tendon fibers. Axially: 1.04, by area: 2.27; by volume: 2.62. Estimate of intrafibrillar volume, assuming 80% of mineral is within fibrils: 0.73 cc/g dry collagen.

In order to determine the nature of tissue repair after removal of condyles, bilateral condylectomies were performed in seven growing female Macaca fascicularis. Two animals underwent condylectomies only, and five animals were fitted with maxillary and mandibular splints before undergoing condylectomies. One condyle from each condylectomized animal was processed for histologic examination. Four animals, with intact condyles, were available as controls: Two had splints placed, while the other two did not undergo any treatment. Nine mo after surgery, the histology of 12 resection sites and 12 control condyles (seven removed at condylectomy and five at death) was compared. In the control condyles, hypertrophic cartilage was seen over the entire condylar surface. From the 12 resection sites, five showed hypertrophic cartilage, non-hypertrophic cartilage cells were present in three, and four demonstrated bone apposition and resorption. Cartilage was present only at the medial and central aspects of the surgical site, and in every specimen, bone was seen at the lateral pole. Two out of 12 fossae overlying surgical sites contained hypertrophic cartilage, while the five control glenoid fossae showed bone, an intermediate zone, and a fibrous capsule. Because of the variety in tissue response and the small number of animals in each group, the effect of the splints could not be determined. Based on the results of this study, the following was concluded: (1) Regeneration of organized hypertrophic cartilage with inherent growth potential can take place after condylectomy, albeit not in every instance and only in the medial aspect of the stump. In the lateral aspect, and also medially if hypertrophic cartilage does not reform, bone is predominant. The original height is not recovered. (2) The cartilage of the glenoid fossa is capable of adaptive changes similar to those seen in condylar cartilage.