Identificación del complejo rojo en la necrosis pulpar abierta y cerrada con técnicas moleculares / Red complex identification in exposed and unexposed necrotic pulp with molecular techniques

Objetivo: identificar el complejo rojo periodontal, formado por Porphyromonas gingivalis, Treponema denticola y Tannerella forsythia, en la infección endodóntica primaria de necrosis pulpar, con cámara abierta y cerrada, utilizando técnicas de reacción en cadena de la polimerasa. Materiales y métodos: se realizó la toma para reacción en cadena de la polimerasa en 27 dientes con necrosis pulpar, 13 con cámara pulpar abierta y 14 con cámara cerrada. Resultados: en las muestras de necrosis abierta se identificaron P. gingivalis en un 92 por ciento, T. denticola en un 76 por ciento, T. forsythia en un 76 por ciento y el complejo rojo en un 61 por ciento. Las tomas de necrosis cerrada mostraron P. gingivalis en un 78 por ciento y T. denticola en un 57 por ciento; no se identificaron T. forsythia ni el complejo rojo. El análisis estadístico evidenció diferencias significativas entre los dos grupos (P<0,05). Conclusión: el sinergismo de las tres bacterias que forman el complejo rojo agravaría la patogénesis de la infección endodóntica y permitiría relacionar la microbiología endodóntica con la microbiología de periodontitis crónica.

Clonality of bacterial consortia in root canals and subjacent gingival crevices.

AIM: No oral niche can be considered to be segregated from the subjacent milieu because of the complex community behavior and nature of the oral biofilms. The aim of this study was to address the paucity of information on how these species are clonally related to the subjacent gingival crevice bacteria. METHODS: We utilized a metagenomic approach of amplifying 16S rDNA from genomic DNA, cloning, sequencing and analysis using LIBSHUFF software to assess the genetic homogeneity of the bacterial species from two infected root canals and subjacent gingival crevices. RESULTS: The four niches studied yielded 186 clones representing 54 phylotypes. Clone library comparisons using LIBSHUFF software indicated that each niche was inhabited by a unique flora. Further, 42% of the clones were of hitherto unknown phylotypes indicating the extent of bacterial diversity, especially in infected root canals and subjacent gingival crevices. CONCLUSIONS: We believe data generated through this novel analytical tool shed new light on understanding oral microbial ecosystems.

Primate pulpal healing after exposure and TheraCal application.

AIM: The purpose of this in vivo study was to compare the effectiveness of a new light cured resin based dicalcium/tricalcium silicate pulp capping material (TheraCalLC, Bisco), pure Portland cement, resin based calcium hydroxide or glass ionomer in the healing of bacterially contaminated primate pulps. STUDY DESIGN: The experiment required four primates each having 12 teeth prepared with buccal penetrations into the pulpal tissues with an exposure of approximately 1.0 mm. The exposed pulps of the primate teeth were covered with cotton pellets soaked in a bacterial mixture consisting of microorganisms normally found in human pulpal abscesses. After removal of the pellet, hemostasis was obtained and the pulp capping agents applied. The light cured resin based pulp capping material (TheraCal LC) was applied to the pulpal tissue of twelve teeth with a needle tip syringe and light cured for 15 seconds. Pure Portland cement mixed with a 2% Chlorhexidine solution was placed on the exposed pulpal tissues of another twelve teeth. Twelve additional teeth had a base of GIC applied (Triage, Fuji VII GC America) and another twelve had a pulp cap with VLC DYCAL (Dentsply), a light cured calcium hydroxide resin based material. The pulp capping bases were then covered with a RMGI (Fuji II LC GC America). The tissue samples were collected at 4 weeks. The samples were deminerilized, sectioned, stained and histologically graded. RESULTS: There were no statistically significant differences between the groups in regard to pulpal inflammation (H = 0.679, P = 1.00). However, both the Portland cement and light cured TheraCal LC groups had significantly more frequent hard tissue bridge formation at 28 days than the GIC and VLC Dycal groups (H = 11.989, P = 0.009). The measured thickness of the hard tissue bridges with the pure Portland and light cured TheraCal LC groups were statistically greater than that of the other two groups (H = 15.849, P = 0.002). In addition, the occurrence of pulpal necrosis was greater with the GIC group than the others. Four premolars, one each treated according to the protocols were analyzed with a microCT machine. The premolar treated with the light cured TheraCal LC demonstrated a complete hard tissue bridge. The premolar treated with the GIC did not show a complete hard tissue bridge while the premolar treated with VLC Dycal had an incomplete bridge. The pure Portland with Chlorhexidine mixture created extensive hard tissue bridging. CONCLUSION: TheraCal LC applied to primate pulps created dentin bridges and mild inflammation acceptable for pulp capping.

Evidence supporting a protective role for th9 and th22 cytokines in human and experimental periapical lesions.

INTRODUCTION: The development of periapical granulomas is dependent on the host response and involves Th1, Th2, Th17, and Treg-related cytokines. The discovery of new Th9 and Th22 subsets, with important immunomodulatory roles mediated by interleukin (IL)-9 and IL-22, respectively, emphasizes the need for reevaluation of current cytokine paradigms in context of periapical lesions. We investigated the expression of IL-9 and IL-22 in active and stable human granulomas and throughout experimental lesion development in mice. METHODS: Periapical granulomas (N = 83) and control specimens (N = 24) were evaluated regarding the expression of IL-9 and IL-22 via real-time polymerase chain reaction. Experimental periapical lesions were induced in mice (pulp exposure and bacterial inoculation) and the lesions evolution correlation with IL-9 and IL-22 expression kinetics was evaluated. RESULTS: IL-9 and IL-22 mRNA expression was higher in periapical lesions than in control samples; higher levels of IL-9 and IL-22 were observed in inactive than in active lesions. In the experimental lesions model, increasing levels of IL-9 and IL-22 mRNA were detected in the lesions, and inverse correlations were found between IL-9 and IL-22 and the increase of lesion area in the different time point intervals. CONCLUSIONS: Our results suggest that Th9 and Th22 pathways may contribute to human and experimental periapical lesion stability.

Inhibiting periapical lesions through AAV-RNAi silencing of cathepsin K.

Dental caries, one of the most prevalent infectious diseases worldwide, affects approximately 80% of children and the majority of adults. Dental caries may result in endodontic disease, leading to dental pulp necrosis, periapical inflammation and bone resorption, severe pain, and tooth loss. Periapical inflammation may also increase inflammation in other parts of the body. Although many studies have attempted to develop therapies for this disease, there is still an urgent need for effective treatments. In this study, we applied a novel gene therapeutic approach using recombinant adeno-associated virus (AAV)-mediated RNAi knockdown of Cathepsin K (Ctsk) gene expression, to target osteoclasts and periapical bone resorption in a mouse model. We found that AAV-sh-Cathepsin K (AAV-sh-Ctsk) impaired osteoclast function in vivo and furthermore reduced bacterial infection-stimulated bone resorption by 88%. Reduced periapical lesion size was accompanied by decreases in mononuclear leukocyte infiltration and inflammatory cytokine expression. Our study shows that AAV-RNAi silencing of Cathepsin K in periapical tissues can significantly reduce endodontic disease development, bone destruction, and inflammation in the periapical lesion. This is the first demonstration that AAV-mediated RNAi knockdown gene therapy may significantly reduce the severity of endodontic disease.

Sexual dimorphism in periapical inflammation and bone loss from mitogen-activated protein kinase phosphatase-1 deficient mice.

INTRODUCTION: Mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) has been shown to be a key negative regulator of the MAPK pathways of the innate immune system. The impact of MKP-1 in an endodontic model has yet to be studied. Thus, the purpose of this study was to determine the role of MKP-1 in a bacterial-driven model of pathologic endodontic bone loss. METHODS: Pulps were exposed in both lower first molars of 10-week-old mkp-1(+/+) and mkp-1(-/-) mice and left open to the oral environment for either 3 or 8 weeks. At death, mandibles were harvested and scanned by micro-computed tomography (µCT) to determine periapical bone loss. Histopathologic scoring was then performed on the samples to determine the amount of inflammatory infiltrate within the periapical microenvironment. RESULTS: Significant bone loss and inflammatory infiltrate were found in all experimental groups when compared with control. No statistical difference was found between mkp-1(+/+) and mkp-1(-/-) at either time point with respect to bone loss or inflammatory infiltrate. At 8 weeks, male mkp-1(-/-) mice were found to have significantly more bone loss and inflammatory infiltrate when compared with female mkp-1(-/-) mice. There was also a significant correlation between an increase in bone loss and increase in inflammatory infiltrate. CONCLUSIONS: A sexual dimorphism exists in the periapical inflammatory process, where male mkp-1(-/-) mice have more inflammation than female mkp-1(-/-) mice. The increase in inflammatory infiltrate correlates to more bone loss in the male mice.

A microbiological profile of unexposed and exposed pulp space of primary endodontic infections by checkerboard DNA-DNA hybridization.

INTRODUCTION: The aim of this study was to evaluate, by checkerboard DNA-DNA hybridization, the composition of the microbiota of primary endodontic infections in cases associated with exposed (n = 30) and unexposed (n = 30) pulp space. METHODS: Samples were collected by means of a #15 H-type file and 2 sterile paper points from 60 single-rooted teeth with necrotic pulp and periapical lesions. The presence, levels, and proportions of 40 bacterial species were determined by checkerboard DNA-DNA hybridization. RESULTS: The species found in higher counts (×10(5)) in exposed pulp space cases were Eubacterium saburreum, Fusobacterium nucleatum ssp. vincentii, Tannerella forsythia, Enterococcus faecalis, Neisseria mucosa, Campylobacter gracilis, and Prevotella nigrescens, and in unexposed pulp space cases they were F. nucleatum ssp. vincentii, N. mucosa, E. faecalis, E. saburreum, C. gracilis, and Porphyromonas gingivalis. Counts of F. nucleatum ssp. vincentii, Campylobacter sputigena, Capnocytophaga showae, Treponema socrenskii, Porphyromonas endodontalis, Eikenella corrodens, and Capnocytophaga ochracea were significantly higher in unexposed pulp space cases (P < .05). CONCLUSIONS: The data of the present investigation suggested specific differences between the composition of the microbiota in cases with exposed and unexposed pulp space and an association between higher levels of some specific species and unexposed pulp space cases.

Bacterial intensity and localization in primary molars with caries disease.

AIM: The aim was to assess the characteristics and outcomes of infections affecting the structures of carious primary molars. MATERIALS AND METHODS: Forty primary molars were used and classified according to the following clinical situation: With profound caries lesion, with bone loss at the furcation region, with perforation of the pulp chamber floor, and residual roots. The teeth were demineralized, cut, and stained with both haematoxylin-eosin and Brown and Brenn staining techniques. Assessment was performed using optical microscopy. RESULTS: Statistical analysis of the data by means of the Chi-square test suggests that there was a significant relationship (P<0.001) between the intensity and localization of infection and the level of destruction of dental structures. A significant difference was also observed in the intensity and localization of infection between the groups regarding crown, furca, and root (P<0.001). CONCLUSION: More intense and profound the infection, more severe is the dental destruction. The groups of residual roots showed the most severe bacterial infection compared to other groups.

Bacteria-reactive immune response may induce RANKL-expressing T cells in the mouse periapical bone loss lesion.

INTRODUCTION: The present study investigated whether bacteria infecting the root canal can activate any infiltrating T cells to produce receptor activator of nuclear factor kappa B (NF-κB) ligand (RANKL). METHODS: Using a mouse model of periapical lesion induced by artificial dental pulp exposure, the presence of RANKL-positive T cells and osteoclasts in the periapical lesion was examined by an immunohistochemical approach. The bacteria colonizing the exposed root canal were identified by 16S ribosomal RNA (rRNA) sequence analysis. The isolated endodontic bacteria were further immunized to normal mice, and soluble activator of NF-κB ligand (sRANKL) production by the T cells isolated from the immunized mice was evaluated by ex vivo culture system. RESULTS: RANKL-positive T cells along with TRAP+ osteoclasts were identified in periapical bone resorption lesions. The gram-negative bacterium Pasteurella pnumotropica, which was most frequently detected from the root canal of exposed pulp, showed remarkably elevated serum immunoglobulin G (IgG)-antibody response in pulp-exposed mice compared with control nontreated mice. Immunization of mice with P. pneumotropica induced not only serum IgG-antibody but also primed bacteria-reactive T cells that produced sRANKL in response to ex vivo exposure to P. pneumotropica. CONCLUSIONS: T cells infiltrating the periapical region express RANKL, and the endodontic bacteria colonizing the root canal appear to induce RANKL expression from bacteria-reactive T cells, suggesting the possible pathogenic engagement of the immune response to endodontic bacteria in the context of developing bone resorptive periapical lesions.

Antimicrobial photodynamic therapy for the treatment of teeth with apical periodontitis: a histopathological evaluation.

INTRODUCTION: This study evaluated the in vivo response of apical and periapical tissues of dogs' teeth with apical periodontitis after one-session endodontic treatment with and without antimicrobial photodynamic therapy (aPDT). METHODS: Sixty root canals with experimentally induced apical periodontitis were instrumented and assigned to 4 groups receiving aPDT and root canal filling (RCF) or not: group aPDT+/RCF+ (n = 20): aPDT (photosensitizer phenothiazine chloride at 10 mg/mL for 3 minutes and diode laser [λ = 660 nm, 60 mW/cm(2)] for 1 minute) and RCF in the same session; group aPDT+/RCF- (n = 10); group aPDT-/RCF+ (n = 20), and group aPDT-/RCF- (n = 10). Teeth were restored, and the animals were killed after 90 days. Sections from the maxillas and mandibles were stained with hematoxylin-eosin and Mallory trichrome and examined under light microscopy. Descriptive (ie, newly formed apical mineralized tissue, periapical inflammatory infiltrate, apical periodontal ligament thickness, and mineralized tissue resorption) and quantitative (ie, periapical lesion size and number of inflammatory cells) microscopic analysis was performed. Quantitative data were analyzed by the Kruskal-Wallis and Dunn tests (α = .05). RESULTS: In the aPDT-treated groups, the periapical region was moderately/severely enlarged with no inflammatory cells, moderate neoangiogenesis and fibrogenesis, and the smallest periapical lesions. CONCLUSIONS: Although apical closure by mineralized tissue deposition was not achieved, the absence of inflammatory cells, moderate neoangiogenesis, and fibrogenesis in the periapical region in the groups treated with aPDT indicate that this can be a promising adjunct therapy to cleaning and shaping procedures in teeth with apical periodontitis undergoing one-session endodontic treatment.

Clonal analysis of the microbiota of severe early childhood caries.

BACKGROUND/AIMS: Severe early childhood caries is a microbial infection that severely compromises the dentition of young children. The aim of this study was to characterize the microbiota of severe early childhood caries. METHODS: Dental plaque samples from 2- to 6-year-old children were analyzed using 16S rRNA gene cloning and sequencing, and by specific PCR amplification for Streptococcus mutans and Bifidobacteriaceae species. RESULTS: Children with severe caries (n = 39) had more dental plaque and gingival inflammation than caries-free children (n = 41). Analysis of phylotypes from operational taxonomic unit analysis of 16S rRNA clonal metalibraries from severe caries and caries-free children indicated that while libraries differed significantly (p < 0.0001), there was increased diversity than detected in this clonal analysis. Using the Human Oral Microbiome Database, 139 different taxa were identified. Within the limits of this study, caries-associated taxa included Granulicatella elegans (p < 0.01) and Veillonella sp. HOT-780 (p < 0.01). The species associated with caries-free children included Capnocytophaga gingivalis (p < 0.01), Abiotrophia defectiva (p < 0.01), Lachnospiraceae sp. HOT-100 (p < 0.05), Streptococcus sanguinis (p < 0.05) and Streptococcus cristatus (p < 0.05). By specific PCR, S. mutans (p < 0.005) and Bifidobacteriaceae spp. (p < 0.0001) were significantly associated with severe caries. CONCLUSION: Clonal analysis of 80 children identified a diverse microbiota that differed between severe caries and caries-free children, but the association of S. mutans with caries was from specific PCR analysis, not from clonal analysis, of samples.

DIAGNOdent laser fluorescence assessment of endodontic infection.

INTRODUCTION: Real-time assessment of the microbial status of the root canal system would be useful in clinical endodontic practice for determining endpoints of biomechanical treatment. This laboratory study used an existing laser fluorescence device, the DIAGNOdent (KaVo, Biberach, Germany), in a proof-of-concept study. METHODS: Visible laser red light (wavelength 655 nm) was used to elicit fluorescence emissions in the near-infrared range from infected and uninfected root canals. A prototype sapphire tip designed for periodontal assessment was used to analyze the pulp chamber and coronal third of the root canal system in extracted teeth. The fluorescence properties of bacterial cultures, monospecies biofilms in root canals, pulpal soft tissues, and sound dentin were also evaluated, together with 50 extracted teeth with known endodontic pathology. RESULTS: Sound dentin and healthy pulpal soft tissue gave an average fluorescence reading of 5 (on a scale of 100), whereas biofilms of Enterococcus faecalis and Streptococcus mutans established in root canals showed a progressive increase in fluorescence over time. Fluorescence readings reduced to the "healthy" threshold reading of 5 when root canals were endodontically treated, and the experimentally created bacterial biofilms were removed completely. High fluorescence readings were recorded in the root canals and pulp chambers of extracted teeth with radiographic evidence of periapical pathology and scanning electron microscopy evidence of bacterial infection. CONCLUSIONS: The use of the DIAGNOdent fluorescence approach for the assessment of the status of the pulp chamber and root canal system holds promise for clinical application; once more, flexible tips can be developed for gaining greater penetration into middle and apical thirds of the root canal.

iNOS-derived nitric oxide modulates infection-stimulated bone loss.

Nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) plays an important role in host defense, as well as in inflammation-induced tissue lesions. Here we evaluated the role of NO in bone loss in bacterial infection-induced apical periodontitis by using iNOS-deficient mice (iNOS(-/-)). The iNOS(-/-) mice developed greater inflammatory cell recruitment and osteolytic lesions than WT mice. Moreover, tartrate-resistant acid-phosphatase-positive (TRAP(+)) osteoclasts were significantly more numerous in iNOS(-/-) mice. Furthermore, the increased bone resorption in iNOS(-/-) mice also correlated with the increased expression of receptor activator NF-kappaB (RANK), stromal-cell-derived factor-1 alpha (SDF-1 alpha/CXCL12), and reduced expression of osteoprotegerin (OPG). These results show that NO deficiency was associated with an imbalance of bone-resorption-modulating factors, leading to severe infection-stimulated bone loss.

Characterization of an ex vivo model for the assessment of root canal disinfection.

Root canal bacteria in teeth with apical periodontitis were enumerated after extraction and incubation. Canals in 36 teeth were sampled after: S1, incubation for 2 hours (group A), 2 days (group B), 4 days (group C), and 6 days (group D); S2, subsequent incubation for 1 week; S3, canal disinfection; and S4, final incubation for 1 week. Bacterial concentrations were determined by culture (colony-forming unit [CFU]) and epifluorescence-microscopy (EFM) and compared by using pairwise and exact-permutation tests (p < 0.05). CFU counts were lower than EFM counts. CFU counts in S1 were higher in Gp(A) than in Gp(C) (p < 0.004) and Gp(D) (p < 0.02). EFM counts in S1 were higher in Gp(A) than in Gp(C) (p < 0.02). Both enumeration methods showed bacterial counts decreasing from S1 to S2 (p < 0.04). EFM was superior to culture in this ex vivo model. The indigenous flora survived incubation for 6 days, but the adverse effect of initial access would preclude testing of disinfection protocols that require two sessions.

Expression of toll-like receptor 2 and 4 in dental pulp.

Toll-like receptors (TLRs) are important factors in innate immune responses because they mediate signals from bacterial cell wall components during inflammatory reactions. However, the role of TLR in dental pulp, which is bounded by hard tissues, is little understood. The present study investigated the expression of TLR-2 and TLR-4 in experimentally inflamed pulp by quantitative real-time polymerase chain reaction and immunohistochemistry. Total RNA isolated from pulp tissue from 0 to 72 hours after bacterial dentinal infection. The TLR-2 messenger RNA (mRNA) level was 30-fold higher than the TLR-4 mRNA level at 9 hours. The TLR-2 mRNA level in pulp began to increase by 3 hours after bacterial infection, reaching a maximum level after 9 hours and gradually decreasing from 9 to 72 hours. Numerous TLR-2- and CD64-positive cells detected on macrophage and dendritic-like cells, TLR-4-positive cells detected a little in the pulp at 9 hours. These results suggest that TLR-2 may be mainly regulated during the early stage of pulp inflammation triggered by bacterial infection.

Equivalency study of histological responses to complete or partial pulpotomies in inflamed baboon immature first permanent molars.

UNLABELLED: Partial pulpotomy is an accepted treatment for traumatised incisor teeth with exposed pulps. Clinical studies in humans suggest that this may also be an acceptable technique for carious exposed pulps in molar teeth, but objective histological evidence to support this perception is lacking. OBJECTIVE: To compare histological responses to complete or partial pulpotomies of inflamed pulps in immature baboon first permanent molar teeth. METHODS: An experimental study in the baboon (Papio ursinus). Pulpitis was induced with fresh Streptococcus mutans placed into occlusal cavities with a small pulpal exposure in 34 first permanent molars of 9 juvenile baboons. After 14 days a pulpotomy, either complete or partial, was performed on the same molars in contra-lateral quadrants using calcium hydroxide covered with IRM and amalgam. After 90 days specimens were harvested and examined under the light microscope with the examiner blind to the treatment. RESULTS: Reaction frequencies in the complete and partial pulpotomy teeth were: dentine bridges 9/16 and 10/16, viable pulp in root canals 10/16 and 13/18, peri-apical abscesses 3/13 and 4/13. Fisher's exact probability test showed no statistically significant rates between the groups. CONCLUSIONS: Complete or partial pulpotomy of inflamed pulps in immature baboon first permanent molars produced comparable reactions.

Effects of a new antibacterial adhesive on the repair capacity of the pulp-dentine complex in infected teeth.

AIM: To evaluate the effects of a self-etching/priming adhesive system, containing the antibacterial monomer 12-methacryloyloxy-dodecylpyridinium bromide (MDPB), on the repair capacity of the pulp-dentine complex in infected cavities in dog's teeth. METHODOLOGY: Class V cavities with a residual dentine thickness ranging from 0.3-0.8 mm were prepared on the buccal surface of permanent teeth in four dogs. Pulpal exposures were performed in half of the cavities. Millipore filters that had been incubated for 3 h in a 10(5) milky suspension of a-streptococci were placed in the cavities, which were then filled temporarily. After 24 h, the filters were removed and both the exposed and non-exposed cavities were washed with sterile saline and assigned to four groups which were treated with either the experimental antibacterial adhesive system, or Clearfil SE bond, Dycal and Teflon discs. Stereotype connective tissue reactions (inflammatory cell response and/or tissue necrosis) and pulp-specific reparative tissue responses (reduction of odontoblasts and tertiary dentine formation) were assessed at post-operative periods of 4 and 8 weeks. RESULTS: Neither severe inflammation nor tissue necrosis was observed, either in the dentinal cavities or pulpal exposures treated with the self-etch adhesive containing MDPB. Rates of tertiary dentine formation in infected dentinal cavities treated with this system were comparable with those observed after dentine treatment with the Ca(OH)2-based material. Dentinal bridging was not seen in pulpal exposures treated with the experimental adhesive. CONCLUSIONS: The new antibacterial adhesive system maintained pulp vitality and primary odontoblastic function in infected nonexposed and exposed cavities but interfered with reparative dentine formation in infected pulpal exposures.

Identification of cultivable microorganisms from primary endodontic infections with exposed and unexposed pulp space.

This study was aimed at comparing the cultivable microorganisms in canals with periapical radiolucencies with exposed and unexposed pulp space. Microbiological samples were taken and analyzed from 45 canals with exposed pulp space, and 43 canals with unexposed pulp space. The canal contents were analyzed by aerobic/anaerobic culture, and conventional identification techniques. There were 211 isolates of bacteria belonging to 28 genera and 55 species recovered from exposed canals. In the unexposed group, 185 isolates of bacteria were recovered, of which 54 species of 28 genera were identified. Among the four most common genera, Prevotella was significantly more common in the exposed group (51/211 in the exposed group versus 30/185 in the unexposed group) (p = 0.049), while there were no differences in prevalence of Actinomyces, Peptostreptococcus, and Campylobacter between two groups of canals. In addition, Fusobacterium nucleatum and Propionibacterium acne were significantly more common in the unexposed canals (p = 0.047 and p = 0.0051, respectively). Similarity in bacterial species in these two groups suggests that pulp space exposure may not be a significant factor in determining the type of bacteria present in infected canals.

Pulpitis induction in baboon primary teeth using carious dentine or Streptococcus mutans.

The objective of this equivalency study was to see if a colony of Streptococcus mutans placed into cavities in primary molar teeth produced pulpitis similar to an established pulpitis induction method using carious dentine. In two juvenile baboons (Papio ursinus), occlusal cavities were cut in all 16 primary molar teeth, followed by making a small pulpal exposure after which the cavity was swabbed with 37 per cent phosphoric acid. In one half of the teeth, fresh soft human carious dentine was placed over the pulpal exposure; in the remaining teeth the exposure was covered with a colony of Streptococcus mutans in agar. All the cavities were restored with unlined light-cured composite resin. After 14 days specimens were harvested and examined under the light microscope with the examiner blind to the induction method. In both groups of teeth there was recognisable pulp, hyperaemia, micro-abscesses in the pulp and peri-apical abscesses. Reactions to soft caries were more severe than to Streptococcus mutans. The results show that Streptococcus mutans placed in a cavity with an exposure produces comparable pulpitis to fresh soft human carious dentine in the same type of cavity and that both methods produce pulpitis suitable for testing pulpotomy or pulpectomy treatments.

Consequences of crown fractures with pulpal exposure: histopathological evaluation in dogs.

When a crown fracture involving pulpal exposure is produced, the therapeutic treatment to be applied depends to a great extent on the general histopathological condition of the exposed pulp. Hence, the objective of this study was to evaluate histopathological and bacteriological changes occurring in dental tissue and periradicular tissue of crown-fractured teeth with pulpal exposure. Twenty-four anterior teeth (central and lateral incisors) from the maxillary teeth of four young, adult Mongrel dogs were used. At 48 and 72 h after performing the crown fractures, the animals were sacrificed and the results evaluated. Both observation periods revealed the existence of an area of superficial inflammation with the formation of hyperplastic tissue towards the external surface. Intense neutrophilic infiltrate was observed below it. Mean depth of inflammation was greater at 48 h (4633.33 microm) than at 72 h (3933.33 microm), perhaps coinciding with the bigger pulp chamber opening (x1332.14 microm at 48 h vs. x479.52 microm at 72 h). Upon approaching the cervical portion, the inflammation became less. Bacterial contamination was constant in all the cases evaluated, worsening the histopathological findings with exposure time. This study demonstrates that when a crown fracture with pulpal exposure is produced, the success in treating it depends partly on how quickly therapeutic treatment is administered.