Periodontitis Exacerbates Benign Prostatic Hyperplasia through Regulation of Oxidative Stress and Inflammation.

Epidemiological studies demonstrate that men with periodontitis are also susceptible to benign prostatic hyperplasia (BPH) and that periodontal treatment can improve the prostatic symptom. However, molecular links of this relationship are largely unknown. The goal of the current study was to elucidate the effects of experimental periodontitis on the hyperplasia of prostate and whether oxidative stress and inflammation participated in this process. For this purpose, ligature-induced periodontitis, testosterone-induced BPH, and the composite models in rats were established. Four weeks later, all the rats were sacrificed and the following items were measured: alveolar bone loss and histological examination of periodontal tissues were taken to assess the establishment of periodontitis model, prostate index and histological examination of prostate tissues were taken to test the establishment of the BPH model, inflammatory cytokines in plasma were assessed, and Bax/Bcl-2 proteins related to cell apoptosis were analyzed via western blot analysis. To further investigate whether oxidative stress participates in the aggravation of BPH, in vitro models were also conducted to measure the production of intracellular reactive oxygen species (ROS) and hydrogen peroxide (H2O2) concentration. We found that simultaneous periodontitis and BPH synergistically aggravated prostate histological changes, significantly increased Ki67 proliferation, and reduced apoptosis in rat prostate tissues. Also, our results showed that periodontal ligation induced increased Bcl-2 protein expression, whereas Bax expression was decreased in BPH rats than in normal rats. Compared with the control group, periodontitis and BPH both significantly enhanced inflammatory cytokine levels of TNF-α, IL-6, IL-1ß, and CRP. Furthermore, Porphyromonas gingivalis lipopolysaccharide induced enhanced generation of intracellular expression of ROS and H2O2 in BPH-1 cells. Our experimental evidence demonstrated that periodontitis might promote BPH development through regulation of oxidative stress and inflammatory process, thus providing new strategies for prevention and treatment of BPH.

The Roles of FOXO1 in Periodontal Homeostasis and Disease.

Periodontitis is an oral chronic inflammatory disease that is initiated by periodontal microbial communities and requires disruption of the homeostatic responses. The prevalence of periodontal disease increases with age; more than 70% of adults 65 years and older have periodontal disease. A pathogenic microbial community is required for initiating periodontal disease. Dysbiotic immune-inflammatory response and bone remodeling are characteristics of periodontitis. The transcription factor forkhead box protein O1 (FOXO1) is a key regulator of a number of cellular processes, including cell survival and differentiation, immune status, reactive oxygen species (ROS) scavenging, and apoptosis. Although accumulating evidence indicates that FOXO1 activity can be induced by periodontal pathogens, the roles of FOXO1 in periodontal homeostasis and disease have not been well documented. The present review summarizes how the FOXO1 signaling axis can regulate periodontal bacteria-epithelial interactions, immune-inflammatory response, bone remodeling, and wound healing.

Chloroquine and 3-Methyladenine Attenuates Periodontal Inflammation and Bone Loss in Experimental Periodontitis.

Periodontitis is an inflammation characterized by alveolar bone resorption caused by imbalance in bone homeostasis. It is known that autophagy is related to inflammation and bone metabolism. However, whether autophagy inhibitors could be used for periodontitis in animal models remains unknown. We investigated the role of two classical autophagy inhibitors, 3-methyladenine (3-MA) and chloroquine (CQ), on the development of rat experimental periodontitis in terms of the bone loss (micro-CT), the number of inflammatory cells (hematoxylin and eosin staining), and the osteoclastic activity (tartrate-resistant acid phosphatase staining). Expression of autophagy-related genes and nuclear factor kappa B p65 (NF-κB p65) were assessed by immunohistochemistry. Expression of Beclin-1 and microtubule-associated proteins 1A/1B light chain 3 (LC3) were analyzed by Western blot. To further observe the effect of autophagy inhibitors on osteoclasts (OCs) in vitro, bone marrow-derived mononuclear macrophages were used. Together, these findings indicated that topical administration of 3-MA or CQ reduced the infiltration of inflammatory cells and alveolar bone resorption in experimental periodontitis. Furthermore, 3-MA and CQ may attenuate activation of OCs by autophagy. Therefore, 3MA and CQ may have prophylactic and therapeutic potential for inflammation and alveolar bone resorption in periodontitis in the future.

Comparison of Clinical and Radiographic Outcomes of Platform-Switched Implants with a Rough Collar and Platform-Matched Implants with a Smooth Collar: A 1-Year Randomized Clinical Trial.

PURPOSE: The aim of this study was to evaluate and compare the clinical and radiographic outcomes of single implants with a platform-switched rough collar (PSRC) and a platform-matched smooth collar (PMSC). MATERIALS AND METHODS: Twenty-six patients missing a tooth in the anterior maxilla (through the premolars) were randomly assigned to the PSRC or the PMSC group. All implants were placed in a flapless approach and restored with an early loading protocol. Clinical measurements were performed at surgery, loading, and at 3, 6, and 12 months after loading. In addition, radiographic evaluations were carried out using standardized periapical radiographs and cone beam computed tomography. Patient satisfaction surveys were completed, and microbial analysis with DNA probes was performed. RESULTS: The implant survival rate was 100% for both groups. The mean marginal bone level (MBL) was significantly higher in the PSRC group compared to the PMSC group at all time points. From the 2-week postoperative visit to 1 year postloading, the mean MBL change in the PSRC group was 0.21 ± 0.56 mm and in the PMSC group it was 0.74 ± 0.47 mm. Soft tissue profiles were stable over time, with no significant differences between groups. There were no significant differences between groups in the number of microbial species seen. Patients in both groups were highly satisfied with postoperative and postprosthetic experiences. CONCLUSION: In this study, the PSRC method preserved marginal bone by a mean of 0.53 mm more than the standard PMSC protocol. Within the limitations of the present study, it can be concluded that the PSRC protocol may be beneficial in marginal bone preservation. Longitudinal studies are needed to verify the long-term effects of this approach.

Arthritis-induced alveolar bone loss is associated with changes in the composition of oral microbiota.

Rheumatoid arthritis (RA) and periodontitis (PD) are chronic inflammatory disorders that cause bone loss. PD tends to be more prevalent and severe in RA patients. Previous experimental studies demonstrated that RA triggers alveolar bone loss similarly to PD. The aim of this study was to investigate if arthritis-induced alveolar bone loss is associated with modification in the oral microbiota. Checkerboard DNA-DNA hybridization was employed to analyze forty oral bacterial species in 3 groups of C57BL/6 mice: control (n = 12; without any challenge); Y4 (n = 8; received oral inoculation of Aggregatibacter Actinomycetemcomitans strain FDC Y4) and AIA group (n = 12; chronic antigen-induced arthritis). The results showed that AIA and Y4 group exhibited similar patterns of bone loss. The AIA group exhibited higher counts of most bacterial species analyzed with predominance of Gram-negative species similarly to infection-induced PD. Prevotella nigrescens and Treponema denticola were detected only in the Y4 group whereas Campylobacter showae, Streptococcus mitis and Streptococcus oralis were only found in the AIA group. Counts of Parvimonas micra, Selenomonas Noxia and Veillonella parvula were greater in the AIA group whereas Actinomyces viscosus and Neisseira mucosa were in large proportion in Y4 group. In conclusion, AIA is associated with changes in the composition of the oral microbiota, which might account for the alveolar bone loss observed in AIA mice.

Porphyromonas gingivalis infection increases osteoclastic bone resorption and osteoblastic bone formation in a periodontitis mouse model.

BACKGROUND: Porphyromonas gingivalis has been shown to invade osteoblasts and inhibit their differentiation and mineralization in vitro. However, it is unclear if P. gingivalis can invade osteoblasts in vivo and how this would affect alveolar osteoblast/osteoclast dynamics. This study aims to answer these questions using a periodontitis mouse model under repetitive P. gingivalis inoculations. METHODS: For 3-month-old BALB/cByJ female mice, 10(9) CFU of P. gingivalis were inoculated onto the gingival margin of maxillary molars 4 times at 2-day intervals. After 2 weeks, another 4 inoculations at 2-day intervals were applied. Calcein was injected 7 and 2 days before sacrificing animals to label the newly formed bone. Four weeks after final inoculation, mice were sacrificed and maxilla collected. Immunohistochemistry, micro-CT, and bone histomorphometry were performed on the specimens. Sham infection with only vehicle was the control. RESULTS: P. gingivalis was found to invade gingival epithelia, periodontal ligament fibroblasts, and alveolar osteoblasts. Micro-CT showed alveolar bone resorption and significant reduction of bone mineral density and content in the infected mice compared to the controls. Bone histomorphometry showed a decrease in osteoblasts, an increase in osteoclasts and bone resorption, and a surprisingly increased osteoblastic bone formation in the infected mice compared to the controls. CONCLUSIONS: P. gingivalis invades alveolar osteoblasts in the periodontitis mouse model and cause alveolar bone loss. Although P. gingivalis appears to suppress osteoblast pool and enhance osteoclastic bone resorption, the bone formation capacity is temporarily elevated in the infected mice, possibly via some anti-microbial compensational mechanisms.

Perialveolar bacterial microbiota and bacteraemia after dental alveolitis in adult rats that had been subjected to neonatal malnutrition.

The aim of the present study was to analyse the bacteriological factors during the process of dental alveolitis, relating it to a higher incidence of bacteraemia in adult rats subjected to neonatal malnutrition. We used forty male Wistar rats, suckled by mothers fed a diet during lactation containing 17 % protein in the nourished group (N) or 8 % protein in the undernourished group (UN). After weaning, the animals were given the Labina standard diet. After 90 d, these animals underwent upper right incisor extraction and induction of alveolitis. The oral microbiota was obtained using a swab and blood culture through venous blood. These procedures were performed before the extraction, 5 min after extraction, on the 21st day after alveolitis for groups N-21 and UN-21 and on the 28th day after alveolitis for groups N-28 and UN-28. Data were expressed as means and standard deviations for parametric data, and as medians and interquartile intervals for non-parametric data. Statistical significance was considered by assuming a critical level of 5 %. Before and after extraction, lower bacterial growth was observed per colony-forming unit (CFU) in the perialveolar region of the upper right incisors of undernourished animals, while the opposite was true after alveolitis, when a larger number of CFU was observed in these animals. The percentage of positive blood cultures obtained after alveolitis was greater in the undernourished animals. The present study thus demonstrated the influence of neonatal malnutrition in the perialveolar microbiota and in the development of bacteraemia after dental alveolitis.

Development of an animal model for Aggregatibacter actinomycetemcomitans biofilm-mediated oral osteolytic infection: a preliminary study.

BACKGROUND: Biofilm-induced inflammatory osteolytic oral infections, such as periodontitis and peri-implantitis, have complex etiology and pathogenesis. A significant obstacle to research has been the lack of appropriate animal models where the inflammatory response to biofilms can be investigated. The aim of this study is to develop a novel animal model to study the host response to Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans)-biofilm colonizing titanium implants. METHODS: Titanium implants were inoculated in vitro with A. actinomycetemcomitans, establishing a biofilm for 1 to 3 days. Biofilm-inoculated and control implants were transmucosally placed into rat hard palate or alveolar ridge. Analysis included documentation of clinical inflammation, polymerase chain reaction, and culture detection of A. actinomycetemcomitans and microcomputed tomography quantitation of peri-implant bone volume. RESULTS: Viable A. actinomycetemcomitans biofilm was successfully established on titanium implants in vitro, detected by confocal laser scanning microscopy. An inflammatory response characterized by clinical inflammation, bleeding, ulceration, hyperplasia, and necrosis was observed around biofilm-inoculated implants. A. actinomycetemcomitans was detected by polymerase chain reaction and culture analysis on 100% of biofilm-inoculated implants for up to 3 weeks and 25% for up to 6 weeks. Microcomputed tomography analysis demonstrated significantly lower bone volume (P <0.05) around biofilm-inoculated implants (29.6% ± 7.6%) compared to non-inoculated implants (50.5% ± 9.6%) after 6 weeks. CONCLUSIONS: These results describe a novel animal model where A. actinomycetemcomitans biofilm was established in vitro on titanium implants before placement in rat oral cavity, leading to an inflammatory response, osteolysis, and tissue destruction. This model may have potential use for investigation of host responses to biofilm pathogens and antibiofilm therapy.

Evaluation of the oral flora in 150 patients suffering from chronic craniofacial pain: a retrospective study.

This study was conducted to determine if microbial infection was a significant factor in patients with undiagnosed craniofacial pain. Of the 150 patients from whom intra-bony cultures were obtained, 23 different groups of isolates were obtained. There were 49 (32.67%) patients whose cultures exhibited growth of microbes other than routine oral flora, mixed skin flora or routine respiratory flora. The most common was of the Streptococcus species (11 or 22.91%) of the 49. Sixty-seven (67) (44.67%) of the total cultures demonstrated the growth of mixed skin flora, nineteen (12.67%) demonstrated the growth of routine respiratory flora and sixteen (10.67%) demonstrated the growth of routine oral flora. No bacterial isolates were found in 16 (10.67%) cultures. The most common histological diagnoses of those who exhibited pathogenic microbial growth were, in order: 1. focal osteoporotic marrow defect; 2. ischemic osteonecrosis; and 3. chronic nonsuppurative osteomyelitis.

Bacterial persistence in dentoalveolar bone following extraction: a microbiological study and implications for dental implant treatment.

BACKGROUND: The microbiological status of apparently healed alveolar bone implant sites is unknown. Implant success may be compromised by site-specific persistence of bacterial biofilm co-aggregations contaminating healed alveolar bone. PURPOSE: The purpose of the present study was to investigate whether extraradicular infection can persist in apparently healed alveolar bone and to develop a surgical debridement strategy that favors implant osseointegration. MATERIALS AND METHODS: The study was conducted on 32 private practice patients. Seventy-seven microbiological samples were taken from 16 pre-implant extraction sockets, 56 healed post-extraction osteotomies at fixture placement, and five failed fixtures. Two of the healed osteotomy samples were healed retreatment sites. Tissue fluid and bone samples were analyzed by either anaerobic/aerobic culturing or DNA molecular techniques. All patients were treated ad modum Brånemark, with a two-stage sterile surgical procedure. A search of the medical and dental literature revealed no evidence-based or best practice recommendations for the use of debridement in implant therapy. Thus, we developed a new technique for the debridement of alveolar bone found to be contaminated by persistent biofilm or planktonic bacteria. RESULTS: The results of the microbiological analysis of 77 bone and effusion samples from 47 implant sites of the 32 patients showed that overall, 32% (n = 25) had bacteria present in the sample. In 16 pre-implant extraction sockets, 69% of samples were positive for the presence of bacteria (n = 11). Of 56 osteotomies with a minimum 3-month healing at fixture placement, 21% revealed a positive culture (n = 12). Two-stage failed fixtures had 100% positive cultures (n = 5) and it was evident from radiographs that all of these failed fixtures had the apical ends close to the former tooth root end. Based on these findings, we have developed a microbiologically based surgical debridement strategy to successfully re-treat early infective failures and to place successful two-stage fixtures. CONCLUSION: Bacteria can persist as a contaminant in apparently healed alveolar bone following extraction of teeth with apical or radicular pathosis. A new technique for surgical debridement to reduce and limit this bacterial contamination has been described.

Decontamination of autogenous bone grafts collected during dental implant site preparation: a pilot study.

Dental implant site preparation produces bone particles that can be used as autogenous bone graft material for the reconstruction of alveolar bone defects; however, collected bone particles are contaminated with oral microorganisms that may cause augmentation failure due to complications associated with infection. The stringent aspiration protocol, preoperative oral chlorhexidine rinsing, and antibiotic prophylaxis were implemented before collecting bone particles. Nonetheless, collected bone particles were still contaminated with bacteria, and, therefore, decontamination of the collected bone particles with chlorhexidine or clindamycin was considered. The aims of this study were to quantitatively determine the degree of bacterial contamination of collected bone particles and to quantitatively evaluate the efficacy of treating collected bone particles with clindamycin or chlorhexidine solutions. Both of the agents effectively decontaminated the collected bone particles. Comparison between these antimicrobials in further studies could be useful in determining which is most effective.

An implant periapical lesion leading to acute osteomyelitis with isolation of Staphylococcus aureus.

A case of an implant periapical lesion (IPL) proceeding to acute osteomyelitis is presented, most likely due to surface contamination of the implant. Five weeks post placement of two anterior mandibular implants, symptoms of acute pain from one implant presented. This symptom and later swelling were unresponsive to antibiotics. On removal of the implant, there was a purulent discharge which, following microbial analysis, proved to be a pure growth of Staphylococcus aureus. A replacement implant was positioned in the site of the previously lost implant ten weeks later, with no recurrence of infection. Staphylococcus aureus can be isolated commonly from the mouths of denture wearers. When an IPL affects a recently placed implant its removal should be accepted but its replacement also considered.

Gingival involvement in oral paracoccidioidomycosis.

BACKGROUND: Paracoccidioidomycosis, a deep mycosis endemic in parts of Latin America, often presents with oral lesions involving the gingiva. Nevertheless, the periodontal literature is devoid of references to oral paracoccidioidomycosis. The purpose of this study was to characterize the gingival involvement in oral paracoccidioidomycosis and to contrast clinical and histopathologic diagnosis of the disease. Differential diagnosis and management of oral paracoccidioidomycosis were reviewed. METHODS: From January 1995 to October 2006, the files of the Oral Pathology Laboratory, School of Dentistry, Alfenas Federal University, were reviewed to identify cases referred because of a clinical diagnosis of oral paracoccidioidomycosis. Data collected included patient demographics (age, gender, race, and occupation), clinical information (oral lesion location), and histopathologic diagnosis. RESULTS: Forty-six cases were identified, and 34 were histopathologically confirmed as paracoccidioidomycosis. Of the remaining 12 cases, one-half were diagnosed as either carcinoma or dysplastic leukoplakia. Of the 34 confirmed paracoccidioidomycosis cases, 45% presented with multiple site involvement, whereas the gingiva/alveolar process was the most prevalent site overall (52%). The gingiva/alveolar process was the most prevalent site in both multiple and single site cases. The majority of patients were men (88%), white (75%), and in their fourth decade of life (47%). Statistical analysis revealed that patients with gingival/alveolar process involvement were demographically indistinguishable from those without. CONCLUSIONS: Oral paracoccidioidomycosis has a strong predilection for the gingiva, whereas patients with gingival lesions do not differ from patients lacking such involvement. Early diagnosis of gingival/oral lesions may prevent life-threatening complications of this mycosis.

Morphometric, histomorphometric, and microcomputed tomographic analysis of periodontal inflammatory lesions in a murine model.

BACKGROUND: Porphyromonas gingivalis is recognized as one of the major periodontal pathogens in chronic periodontitis, a common infectious disease characterized by inflammation and destruction of periodontal tissues. Several animal models with P. gingivalis have been used in periodontitis studies. Additionally, multiple approaches have also been applied to measuring alveolar bone loss in periodontitis models, including histomorphometry, morphometry, and radiography. The aims of this study were to assess periodontal inflammatory lesions after P. gingivalis-induced periodontitis and use this model to compare three approaches for assessing alveolar bone loss. METHODS: Twelve-week-old male C57BL/6 mice were divided into two groups: 48 P. gingivalis-infected and 52 untreated control mice. Periodontitis was induced by wrapping P. gingivalis-soaked ligatures around the left maxillary second molar and changing the ligatures every other day. Mice were euthanized on days 0, 3, 7, and 10 after ligature placement, for a total of 12 experimental and 13 control mice per time point. Epithelial downgrowth, inflammation, and osteoclast activity were evaluated; alveolar bone loss was determined by histomorphometry, morphometry, and microcomputed tomography. RESULTS: The P. gingivalis-infected group showed significantly increased epithelial downgrowth (P <0.05), inflammation (P <0.05), alveolar bone loss (P <0.05), and osteoclast activity (P <0.05) throughout the experimental period compared to the controls. All three methods yielded efficient evaluation of alveolar bone loss. CONCLUSIONS: Our results show evidence that the P. gingivalis-soaked ligature-induced murine model mounts an adequate inflammatory response and exhibits periodontal tissue breakdown compatible with other models of periodontal disease. In addition, alveolar bone loss can accurately be quantified using any of the three alveolar bone analyses presented in this article.

Bacterial contamination of filtered intraoral bone chips.

Intraoral bony defects can be filled with bony particles that are collected in a titanium filter. The aim of this study was to determine quantitatively and qualitatively the degree of this contamination. Over a period of 3 months, bony particles were collected from 50 patients undergoing oral surgery. The bony particles were scraped off the filter, resuspended, and incubated aerobically and anaerobically on human blood agar media. Colony forming units (CFU) were determined as well as the most common species of bacteria. All samples showed anaerobic and aerobic growth. After anaerobic incubation in 44 samples the number of bacteria was higher (38) or equal (six) to that after aerobic incubation. On average, 435,000 CFU (aerobic) and 1,013,000 CFU (anaerobic) per sample were found. The most frequently identified bacteria belonged to Veillonella spp. in the anaerobic and to Streptococcus oralis in the aerobic cultures. In 43 samples black-pigmented colonies were detected. Only bacteria common in the oral cavity were identified. Prophylactic antibiotic therapy may be indicated when using filtered bony particles for intraoral augmentation procedures.

[Microflora on mucosa under different pontics of fixed partial bridge].

OBJECTIVE: To investigate the influence of three pontic types on alveolar ridge mucosal microecosystem. METHODS: Sixty patients ready to accept three unit metal ceramic bridges were selected. The bacterial type and the cultivable flora were counted and the proportions of bacteria detected on the top of alveolar ridge mucosal contact area before tooth preparation and three months after bridge insertion. RESULTS: Type and CFU of bacteria on the alveolar ridge mucosa under modified base-type pontics and modified ridge lap pontics increased significantly (P < 0.05); while there was no significant change under the ovata pontics (P > 0.05). Before tooth preparation and 3 months after fixed prosthesis insertion, the percentages of oral Streptococci and Neisseriae changed significantly (P < 0.05). CONCLUSIONS: The ovata pontic had less influence on mucosal microecosystem than the other two pontics and is the appropriate pontic design for clinical dentist.

[Bacterial contamination of bony particles from the bone collection trap]. / Bakterielle Belastung von Bohrspänen aus dem Knochenfilter.

Intraoral bony defects can be filled with bony particles that are collected in a titanium filter while drilling. The rinsing liquid is contaminated with blood and saliva which implies that the bony particles are also contaminated with bacteria. The aim of this study was to determine quantitatively and qualitatively the degree of this contamination. Over a period of three months bony particles were collected from 50 patients undergoing surgery. The bony particles were scraped off the filter, resuspended and incubated aerobically and anaerobically on human blood agar media. Colony forming units (CFU) were determined as well as the most common species of bacteria. All samples showed anaerobic and aerobic growth. After anaerobic incubation in 44 samples the number of bacteria was higher (38) or equal (six) to that after aerobic incubation. On average 435,000 CFU (aerobic) and 1,013,000 CFU (anaerobic) per sample were found. The most frequently identified bacteria belonged to Veillonella spp. in the anaerobic and to Streptococcus oralis in the aerobic cultures. In 43 samples black pigmented colonies were detected. There were only bacteria identified which are common in the oral cavity.

Association of Streptococcus mutans infection and oral developmental nodules in pre-dentate infants.

Since dental caries may present soon after tooth eruption, we hypothesized that colonization of Streptococcus mutans can occur in the predentate stages. In this study, we examined S. mutans colonization and its association with oral developmental nodules (Bohn's nodules) in 60 pre-term and 128 full-term, three-month-old infants. Overall, S. mutans was cultured from 30% (56/188) of the infants, and oral developmental nodules were noted in 55% (103/188). Compared with the pre-term, full-term infants showed a higher prevalence of S. mutans (34% vs. 20%, p < 0.02) as well as developmental nodules (61% vs. 42%, p < 0.05). In both groups, S. mutans was positively associated with numbers of developmental nodules in a dose-response relationship (p < 0.001), and with maternal salivary levels of the bacteria (p = 0.03). The permanence of S. mutans infection was confirmed by repeat saliva sampling at 6 months of age. Our results thus showed that many infants have already acquired S. mutans at 3 months of age, prior to tooth eruption.

[Effect of antiseptic treatment of alveolar surgical wounds on bacterial growth on cotton suture threads]. / Efeito da anti-sepsia da ferida cirúrgica alveolar sobre o crescimento bacteriano em fios de sutura de algodão.

The objective of this study was to evaluate bacterial growth on cotton suture. The efficiency of cetylpyridinium chloride (50%), hydrogen peroxide (3%) and chlorhexidine (0.12%) in antisepsis was investigated. For that, 20 patients who were submitted to extraction of impacted lower third molars were studied. Five days after extraction, samples were obtained from the oral and alveolar sides of the sutures, before and after antisepsis of the wounds, and were submitted to bacteriological analysis. Bacterial growth was observed in all examined samples. The number of streptococci decreased after antisepsis and there were no statistically significant differences between the methods of antisepsis used.