Randomized Clinical Study of the Use of MTA and Biodentine™ for Pulpotomy in Primary Teeth

ABSTRACT Objective: To verify, through clinical and radiographic evaluations, the in vivo response of the dentin-pulpal complex of human primary teeth after pulpotomy with MTA and Biodentine™ in a follow-up period of 3, 6, and 12 months. Material and Methods: Thirty teeth were divided into MTA pulpotomy (n = 15) and Biodentine™ pulpotomy (n = 15) from children between 5 and 9 years of age, a randomized clinical trial with simple random sampling. The materials were inserted into the cavity after opening and removing the coronary pulp tissue. The cavity base consisted of glass ionomer cement and light-cured composite resin restoration. Clinical and radiographic analyses were performed after 3, 6, and 12 months. Statistical analysis by Fisher's exact test for dichotomous data at a 5% significance level was utilized. Results: Both materials caused color change after 12 months. However, MTA showed a higher percentage than Biodentine™ (p<0.0001). Pain was detected only with Biodentine™ at six months and mobility at 12 months (p=0.0013). Radiographically, after 12 months, periapical lesions, interradicular lesions, and internal resorption were evidenced in 13% of the cases for Biodentine™-treated teeth (p<0.0013). MTA induced pulp calcification in 13% of cases, unlike Biodentine™ (p<0.0013). Conclusion: BiodentineTM and MTA are suitable for clinical use in pulpotomy treatment, yet both materials lead to tooth discoloration.

Gene expression data of inflammatory mediators in apical periodontitis in 129 (wild type) and 5-lipoxygenase knockout mice.

Apical periodontitis is an immune inflammatory response around periapical tissues as a result of pathogens invasion into the root canal. The host immunoinflammatory response could determine the progression of this disease, which involves the recruitment of immune cells, and the release of several cytokines in the lesion site. The 5-lipoxygenase pathway has been activated in some osteolytic diseases due to its capacity to interfere in the proliferation and differentiation of bone cells, including the osteoclasts. As mean to understand the inflammatory genes regulation in the apical periodontitis progression, we evaluated the network of 66 genes related to cytokines, chemokines and other inflammatory mediators and receptors in the wild-type (WT) and 5-lipoxygenase enzyme genetically deficient mice (KO). This article presents data not published but related to the research article "Effects of 5-lipoxygenase gene disruption on inflammation, osteoclastogenesis and bone resorption in polymicrobial apical periodontitis" .

Effect of non-steroidal anti-inflammatory drugs on pulpal and periapical inflammation induced by lipopolysaccharide.

OBJECTIVES: The objective of this study was to evaluate the effect of non-steroidal anti-inflammatory drugs (NSAIDs) in controlling pulpal and periapical inflammation in vivo as a potential coadjutant systemic therapy for pulpitis. MATERIALS AND METHODS: A suspension containing E. coli lipopolysaccharide (LPS; 1.0 µg/µL) was inoculated into the pulp chamber of the first molars of C57BL/6 mice (n = 72), and the animals were treated daily with indomethacin or celecoxib throughout the experimental periods. After 7, 14, 21, and 28 days, the tissues were removed for histopathological, histoenzymology, histometric, and immunohistochemical evaluation. RESULTS: Inoculation of LPS into the pulp chamber induced the synthesis of the enzyme cyclooxygenase-2 (COX-2) in dental pulp and periapical region. Indomethacin and celecoxib treatment changed the profile of inflammatory cells recruited to dental pulp and to the periapex, which was characterized by a higher mononuclear cell infiltrate, compared to LPS inoculation alone which recruited a higher amount of polymorphonuclear neutrophils. Administration of indomethacin for 28 days resulted in the development of apical periodontitis and increased osteoclast recruitment, unlike celecoxib. CONCLUSIONS: NSAIDs indomethacin and celecoxib changed the recruitment of inflammatory cells to a mononuclear profile upon inoculation of LPS into the pup chamber, but indomethacin enhanced periapical bone loss whereas celecoxib did not. CLINICAL RELEVANCE: Celecoxib, a selective COX-2 inhibitor, can change the profile of inflammatory cells recruited to the dental pulp challenged with LPS and might a be potential systemic coadjutant for treatment of pulpitis.