This investigation studied relative changes in periodontal conditions of 18 insulin‐dependent diabetic patients. Measures of gingival inflammation, crevicular fluid aspartate aminotransferase (AST) levels, probing depth and attachment levels, the presence of three periodontal pathogens (Porphyromonas gingivalis, Bacteroides forsythus, and Actinobacillus actinomycetemcomitans) and serum antibody titers to these bacteria, and blood sugar levels (glycosylated hemoglobin, HbAlc) were studied before and 2 months after non‐surgical debridement. Antibody titers to the same bacteria were also studied in sera from 18 sex‐ and age‐matched periodontally healthy and non‐diabetic subjects. Periodontal conditions showed significant improvement. The mean probing depth at 4 of the worst sites selected in each patient decreased from 5.7 mm to 4.8 mm (P < 0.0001). The mean full width probing depth changed from 2.9 mm (s.d. ± 0.2) to 2.5 mm (s.d. ± 0.3). A mean gain of 0.4 mm attachment level was recorded (P < 0.0001). The mean AST value decreased from 1009 μIU to 518 μIU (P < 0.006). Minimal differences in mean glycosylated hemoglobin values (HbAlc) were noticed before and after treatment. A. actinomycetemcomitans was never detected. P. gingivalis was present at 7% of the sites both before and after treatment. B. forsythus was found at 29% of sites (50% of patients) before and at 36% of sites (61% of patients) after treatment. Positive associations were found between the presence of B. forsythus and AST values, gingival index, probing depth, and attachment level (P < 0.05). Baseline serum IgG titers to P. gingivalis were significantly lower in the patients with diabetes (9.5 ELISA units vs. 28.5 ELISA units in the healthy controls). IgG titers to B. forsythus did not differ between diabetic and non‐diabetic subjects. No changes in IgG titers occurred after treatment. Clinical improvements after mechanical non‐surgical therapy in patients with insulin‐dependent diabetes mellitus were modest after 2 months. Treatment did not eliminate B. forsythus and P. gingivalis and did not affect IgG titer responses. More intense therapy, and longer follow‐up times, may be necessary to see more pronounced clinical and systemic effects. J Periodontol 1996;67:794–802.

The objective of this study was to investigate the use of alginate hydrogels to present either exogenous or endogenous transforming growth factor (TGF)-beta 1 to the dentin-pulp complex to signal reparative processes. Hydrogels were prepared, applied to cultured human tooth slices and the effects on tertiary dentinogenesis examined histologically. Both TGF-beta 1-containing and acid-treated alginate hydrogels, but not untreated hydrogels, upregulated dentin matrix secretion and induced odontoblast-like cell differentiation with subsequent secretion of regular tubular dentin matrix on cut pulpal surfaces. It is concluded that TGF-beta 1 can signal both induction of odontoblast-like cell differentiation and upregulation of their matrix secretion in the human dentin-pulp complex. Alginate hydrogels provide an appropriate matrix in which dental regeneration can take place and may also be useful for delivery of growth factors, including TGF-beta s, to enhance the natural regenerative capacity of the dental pulp.

No abstract

Age of the patient affects dentin repair capacity and may be a factor in treatment planning decisions. Minimizing the cutting of dentin, especially the width and base of the preparation, reduces the probability of recurrent pulpal complications.

Mast cells have been shown to be present in substantial numbers in both nonkeratinizing and keratinizing odontogenic cysts and could be seen in the connective tissue capsule and the epithelial lining. Within the cyst capsule, mast cells were more prevalent just beneath the epithelium than in deeper areas. This distribution pattern for mast cells is in accord with the histochemical picture for heparin staining in odontogenic cysts. In the non-keratinizing cysts, there appeared to be some trend towards mast cells being associated with increasing inflammation but not in the odontogenic keratocyst. No evidence could be found for distinct mast cell subpopulations in odontogenic cysts. The presence of mast cells in odontogenic cyst could contribute to their pathogenesis in several ways.