Radiographic and histological evaluation of the treatment of inflamed dental pulps.
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This study compared the pulpal responses to two innovative semihydrous glass ionomer luting cements (STA and ZIN) with those previously obtained for a conventional anhydrous glass ionomer luting cement, Aquacem. ZIN contained zinc oxide in the formulation. The study was conducted according to the BSI (1989) recommendations for testing restorative materials in vivo. ZIN was associated with minimal pulpal changes and microbial microleakage, and differed little from the control material, Kalzinol. The pulpal response to STA was similar to that observed for Aquacem, but was associated with less microbial microleakage. The statistical model demonstrated a significant association between bacterial presence within the experimental cavity and pulpal inflammation. The closer that bacteria were to the pulp, the more severe was the ensuing inflammation.
The pulpal reaction associated with a composite resin alone and composite resin used in conjunction with two dentine bonding agents was studied. Class V cavities were prepared on the labial surfaces of the canine teeth of 18 male ferrets. After acid etching of the enamel margins, the cavities were restored with either a composite resin alone or in combination with one of two dentine bonding agents, Scotchbond and Gluma. One cavity in each animal was filled with Kalzinol as a control. The animals were killed after 7, 14 and 28 days. After histological processing, the pulpal changes were assessed qualitatively and quantitatively according to standard criteria. There were variations in the pulpal response at all time intervals. The responses to the two dentine bonding agents were similar to those found with composite resin alone. No pulpal inflammation was observed in the control teeth. Gram-positive micro-organisms were identified at the interface of restoration and cavity wall, or within the dentinal tubules in virtually all cases in which pulpal inflammation was observed.
A series of studies has been conducted in which monoinfected gnotobiotic rats were used to study the responses of the dental pulp to micro-organisms isolated from carious lesions in dentine. In this study pulp responses to L. plantarum (formerly odontolyticus) (NCTC 1406) in pure culture and in combination with S. mutans (NCTC 10919) are reported. The incidence of inflammation/necrosis/dentine bridge formation observed in animals monoinfected with L. plantarum was similar to that reported in previous germ-free studies. There was a greater incidence of dentine bridge formation in rats monoinfected with L. plantarum compared with those monoinfected with S. mutans. When the two organisms were combined, periapical inflammation was observed in 14% of the teeth examined after 28 days, but there was no significant difference in the incidence of dentine bridge formation. Considerable variation in the density of staining of the two microorganisms in histological sections was observed.
The pulpal response to and cariogenicity of a third strain of Streptococcus mutans, namely S. mutans (NCTC 10832), was studied in monoinfected gnotobiotic rats of the Fischer strain using the techniques described previously by the present authors. Unlike S. mutans (NCTC 10449 and 10919), S. mutans (NCTC 10832) was associated with the presence of inflammatory cell infiltrates in the coronal pulp of a small number of teeth and extensive periapical inflammation 28 days after the creation of untreated pulpal exposures. S. mutans (NCTC 10832) was associated with the presence of extensive pulpal necrosis and reduced dentine bridge formation. These changes were similar to those noted with the other two strains of S. mutans. S. mutans (NCTC 10832) was non-cariogenic in monoinfected gnotobiotic rats of the Fischer strain.
Progression of periodontitis is currently thought to occur during bursts of activity, followed by periods of remission, when healing may occur. This concept contrasts with the older hypothesis that periodontitis was continuously, but slowly, progressive throughout life. At present, there is no proof of the conventional (microbiological) hypothesis which gives a major role to site-specific bacteria in the initiation of bursts of attachment loss. An alternative hypothesis is presented in this paper which accounts for periodontal attachment loss by pathways that are independent of plaque. Severe lesions of the periodontium caused by pulpal pathoses (apical and retrograde periodontitis) are known to form at any level of the periodontium, not only at the root apex. When these lesions cause destruction of the periodontal tissues at the alveolar crest, and when plaque, calculus and gingivitis are also present, an endodontic origin is rarely suspected. Three pathways are proposed to account for the development of localized periodontal attachment loss consequent to pulpal disease. This hypothesis accounts for the sudden deterioration of periodontal sites under regular review, the strict localization of alveolar defects with normal alveolar bone immediately adjacent, the presence of site-specific bacteria (secondary colonizers of deep pockets) which cannot cause disease when transferred to healthy sites, and the antibody responses directed against them.
Patients attending a dedicated dental clinic during the previous 24 months were assessed for the success of root canal treatment. Two groups, totalling 48 patients, had root canal treatment to 57 teeth performed by one operator. All treatment was carried out without antibiotic prophylaxis over two or more appointments. Patients with HIV infection had root canal treatment to 40 teeth. Sixteen patients in the control group had root canal treatment to 17 teeth. Short-term success was determined by follow-up appointments 1-3 months following obturation. No complications were experienced in either group, except with one HIV infected patient. The results of this clinical study indicate that root canal treatment can be carried out following standard procedures and without antibiotic prophylaxis.