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PubMedDate not supplied

Tunnel defects in dentin bridges: their formation following direct pulp capping.

This study was conducted to observe the formation and nature of tunnel defects in dentin bridges, assess the nature of the associated soft tissue elements, and note the relationship of pulp inflammation and necrosis associated with these defects. A total of 235 teeth with class 5 cavity preparation exposures were randomly distributed throughout the dentitions of 14 adult rhesus monkeys. Each pulp was exposed and left open to the oral microflora at one of four time intervals, flushed with saline, debrided, capped with one of two hard-set calcium hydroxide medicaments [Ca(OH)2 (Dycal or Life)] and restored with a dispersed-phase amalgam alloy. Observation times were 14 days, 5 weeks, and 1 and 2 years. A total of 192 dentin bridges formed against the Ca(OH)2 medicaments Life or Dycal in 235 pulp-capped teeth. Considering all four capping periods, 89% of all dentin bridges contained tunnel defects (172 of 192). Forty-one percent (78) of the 192 dentin bridges were associated with recurring pulp inflammation or necrosis and were always associated with the presence of inflammatory cells and stained bacterial profiles. This study demonstrates that a statistically significant number of dentin bridges contain multiple tunnel defects, most of which appear to remain patent. These patent tunnels fail to provide a hermetic seal to the underlying pulp against recurring infection due to microleakage. Most Ca(OH)2 medicaments have been reported to disintegrate and wash out after 6 months, leaving a void underneath the restoration and thereby a pathway for bacterial infection. This study reemphasizes the need to employ biologically relevant measures that will provide a long-term clinical seal against microleakage following direct pulp capping with Ca(OH)2 medicaments alone.

Animals↗
PubMed1979

Bacteria and pulpal reactions under silicate cement restorations.

Silicate cement was inserted in deep unlined cavities in 70 human teeth; 35 cavities were cleaned with an antibacterial cleanser, and the other 35 cavities in the contralateral teeth were treated with water spray only. In all teeth, invasion of bacteria from the tooth surface was prevented with a surface seal. Histologic examinations after 4 weeks revealed bacterial growth on dentinal walls in 9 of the uncleaned and in 2 cleaned cavities. Only in these 11 teeth was an inflammatory reaction seen in the pulp. Under eight cavities without bacterial growth and with silicate cement placed directly on an exposed pulp, no serious injury and no inflammatory reactions were observed. It was concluded that silicate cement per se does not seriously irritate the pulp. Infection of cavity walls should be avoided, not only by removing grinding debris and antibacterial cleansing, but also by use of a liner to prevent invasion of bacteria from the surface of the tooth.

Anti-Bacterial Agents↗
PubMed2005

Pulpal responses following direct pulp capping of healthy dog teeth with dentine adhesive systems.

OBJECTIVE: The aim of the present study was to evaluate the pulpal responses following direct pulp capping of mechanically exposed teeth with new dentine adhesive systems, in the preclinical model of dog teeth. METHODS: Class V cavities (approximately 2.50 mm wide, 3.00 mm long, 1.5-2.0 mm deep) were prepared on the buccal surface of permanent maxillary and mandibulary molars, two rooted premolars, canines and third incisors. The cavities were assigned to five experimental groups, representing one control group treated with a Ca(OH)2-based material and four experimental groups where the adhesive systems Clearfil SE Bond, Prompt-L-Pop, Etch & Prime 3.0 and Single Bond were tested. The pulpal tissue responses to dentine adhesives were assessed at post-operative periods of 7, 21, 65 days. RESULTS: Variable responses were recorded, which were characterized by moderate to severe inflammatory reactions, progressive extension of tissue necrosis with time and total absence of continuous hard tissue bridge formation after pulp capping with each of the four adhesive systems. Application of a Ca(OH)2-based material was characterized by inflammatory cell infiltration, limited tissue necrosis as well as partial to complete hard tissue bridging. CONCLUSIONS: It seems evident that application of dentine adhesive systems in direct contact with the mechanically exposed pulp of healthy dog teeth cannot lead to acceptable repair of the dentine-pulp complex e.g. wound healing with tertiary dentine bridge formation.

Animals↗
PubMed1996

Immunohistochemical detection of prostaglandins E2, F2 alpha, and 6-keto-prostaglandin F1 alpha in experimentally induced periapical inflammatory lesions in rats.

The immunohistochemical localization of prostaglandin (PG) E2, PGF2 alpha, and 6-keto-PGF1 alpha (a stable metabolite of PGI2) was demonstrated in rat periapical inflammatory lesions induced by opening the pulp chamber. Two wk postoperatively, suppurative periapical lesions were formed, and active bone resorption was seen surrounding these lesions. Immunohistochemical examination showed that macrophages infiltrating in inflammatory tissue were positively stained for the examined PGs. In some lesions, wherein acute inflammatory changes subsided and proliferation of fibroblasts started, the fibroblasts were positively stained for 6-keto-PGF1 alpha. Osteocytes and osteoblasts were also positive for 6-keto-PGF1 alpha not only in experimental animals, but also in untreated animals. However the staining intensity of the PG in these cells was higher in periapical lesions than in normal condition. These findings suggested that the cellular sources of the PGs in the periapical lesions are mainly macrophages and fibroblasts, and that the PGs produced by these cells, and possibly osteoblast and osteocytes, may contribute to the osteolytic resorption of periapical lesions.

6-Ketoprostaglandin F1 alpha↗
PubMed2002

Effect of treatment delay upon pulp and periodontal healing of traumatic dental injuries -- a review article.

Based on an analysis of the literature concerning parameters influencing the prognosis of traumatic dental injuries, few studies were found to have examined possible relationships between treatment delay and pulpal and periodontal ligament healing complications. It has been commonly accepted that all injuries should be treated on an emergency basis, for the comfort of the patient and also to reduce wound healing complications. For practical and especially economic reasons, various approaches can be selected to fulfill such a demand, such as acute treatment (i.e. within a few hours), subacute (i.e. within the first 24 h), and delayed (i.e. after the first 24 h). In this survey the consequences of treatment delay on pulpal and periodontal healing have been analyzed for the various dental trauma groups. Applying such a treatment approach to the various types of injuries, the following treatment guidelines can be recommended, based on our present rather limited knowledge of the effect of treatment delay upon wound healing. Crown and crown/root fractures: Subacute or delayed approach. Root fractures: Acute or subacute approach. Alveolar fractures: Acute approach (evidence however questionable). Concussion and subluxation: Subacute approach. Extrusion and lateral luxation: Acute or subacute approach (evidence however questionable). Intrusion: Subacute approach (evidence however questionable). Avulsion: If the tooth is not replanted at the time of injury, acute approach; otherwise subacute. Primary tooth injury: Subacute approach, unless the primary tooth is displaced into the follicle of the permanent tooth or occlusal problems are present; in the latter instances, an acute approach should be chosen. These treatment guidelines are based on very limited evidence from the literature and should be revised as soon as more evidence about the effect of treatment delay becomes available.

Alveolar Process↗