Biphasic calcium phosphate (BCP) bioceramics belong to a group of bone substitute biomaterials that consist of an intimate mixture of hydroxyapatite (HA), Ca(10)(PO(4))(6)(OH)(2), and beta-tricalcium phosphate (beta-TCP), Ca(3)(PO(4))(2), of varying HA/beta-TCP ratios. BCP is obtained when a synthetic or biologic calcium-deficient apatite is sintered at temperatures at and above 700 degrees C. Calcium deficiency depends on the method of preparation (precipitation, hydrolysis or mechanical mixture) including reaction pH and temperature. The HA/beta-TCP ratio is determined by the calcium deficiency of the unsintered apatite (the higher the deficiency, the lower the ratio) and the sintering temperature. Properties of BCP bioceramics relating to their medical applications include: macroporosity, microporosity, compressive strength, bioreactivity (associated with formation of carbonate hydroxyapatite on ceramic surfaces in vitro and in vivo), dissolution, and osteoconductivity. Due to the preferential dissolution of the beta-TCP component, the bioreactivity is inversely proportional to the HA/beta-TCP ratio. Hence, the bioreactivity of BCP bioceramics can be controlled by manipulating the composition (HA/beta-TCP ratio) and/or the crystallinity of the BCP. Currently, BCP bioceramics is recommended for use as an alternative or additive to autogeneous bone for orthopedic and dental applications. It is available in the form of particulates, blocks, customized designs for specific applications and as an injectible biomaterial in a polymer carrier. BCP ceramic can be used also as grit-blasting abrasive for grit-blasting to modify implant substrate surfaces. Exploratory studies demonstrate the potential uses of BCP ceramic as scaffold for tissue engineering, drug delivery system and carrier of growth factors.

The use of biomaterials to replace lost bone has been a common practice for decades. More recently, the demands for bone repair and regeneration have pushed research into the use of cultured cells and growth factors in association with these materials. Here we report a novel approach to engineer new bone using a transient cartilage scaffold to induce endochondral ossification. Chondrocyte/chitosan scaffolds (both a transient cartilage scaffold— experimental—and a permanent cartilage scaffold—control) were prepared and implanted subcutaneously in nude mice. Bone formation was evaluated over a period of 5 months. Mineralization was assessed by Faxitron, micro computed tomography, backscatter electrons, and Fourier transform infrared spectroscopy analyses. Histological analysis provided further information on tissue changes in and around the implanted scaffolds. The deposition of ectopic bone was detected in the surface of the experimental implants as early as 1 month after implantation. After 3 months, bone trabeculae and bone marrow cavities were formed inside the scaffolds. The bone deposited was similar to the bone of the mice vertebra. Interestingly, no bone formation was observed in control implants. In conclusion, an engineered transient cartilage template carries all the signals necessary to induce endochondral bone formation in vivo.

Differences in periodontal disease prevalence, severity, subgingival microflora and host immune response have been reported for various ethnic/racial groups, which implies that risk factors for destructive periodontal disease progression may also vary in these populations. As it is possible that these differences may be due to confounding variables other than ethnicity/race, we have measured serum IgG antibody response to six periodontal pathogens, and compared these data with microbiological, clinical and demographic parameters in three urban minority populations. The study population consisted of 23 Asiatic, 48 African-American and 37 Hispanic subjects, who were resident in the greater New York region. Clinical indices that were recorded included pocket depth, attachment level, gingival erythema, bleeding upon probing, suppuration and supragingival plaque. Attachment level measurements were taken twice at each visit, and the difference between the means of pairs of measurements taken at baseline and two months later was used to determine disease progression. Subgingival microbiological species were identified and enumerated using DNA-DNA checkerboard hybridization. Serum IgG antibody levels to Actinobacillus actinomycetemcomitans serotyopes a and b, Bacteroides forsythus, Campylobacter rectus, Porphyromonas gingivalis and Prevotella intermedia were measured by enzyme-linked immunosorbant assay (ELISA). Mean serum IgG antibody to P. gingivalis was found to be higher in the African-American group, while IgG antibody to B. forsythus was lower in the Hispanic group. However, the African-American group also had greater mean probing depth, attachment loss, number of missing teeth and numbers of individuals within the unskilled occupational group. When the data were analyzed by occupational status, mean serum IgG antibody to P. gingivalis increased from professional to skilled to unskilled groups. For the entire study population, prior disease and subsequent attachment loss were associated with elevated serum IgG antibody to P. gingivalis. Increasing pocket depth, attachment level, gingival erythema and age were also positively correlated with serum IgG antibody to P. gingivalis, but not with serum IgG antibody to the other five subgingival species. No correlation was found between whole-mouth bacterial levels and homologous serum IgG antibody levels. These results suggest that elevated serum IgG antibody to P. gingivalis reflects destructive periodontal disease status, and may be considered a risk factor for disease progression in these ethnic/racial populations. In addition, although differences in serum IgG antibody profiles to subgingival species were found among the three ethnic/racial groups, environmental and socioeconomic variables may have a greater influence on serum IgG antibody levels in these populations.

Although greater destructive periodontal disease prevalence and severity were found in the African-American group, these results suggest that environmental and demographic variables, such as occupational status, may have a greater influence on risk indicators associated with disease prevalence and progression in these populations.

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