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Aim: Periodontal disease encompasses gingivitis and periodontitis, which exerts systemic effects. We conducted a population-based study to evaluate the association between periodontal disease and the risk of cancer., Methods: We used insurance claims data from 1997 to 2010, accessing a database of 1 million randomly selected insurants in Taiwan. All patients were older than 20 and newly diagnosed with periodontitis between 1 January 1997 and 31 December 2010. The comparison cohort comprised patients older than 20, who were newly diagnosed with gingivitis in the same period. Both cohorts were followed until a cancer diagnosis, lost to follow-up, death, termination of insurance, or the end of 2010., Results: The incidence rate of cancer was 1.14 times higher in the study cohort than in the comparison cohort [confidence interval (CI) = 1.11-1.17]. The adjusted hazard ratio (HR) was 1.05 (95% CI = 1.00-1.11). A multivariable analysis showed that the periodontitis patients exhibited an elevated risk of developing oral cancer (adjusted HR = 1.79, 95% CI = 1.42-2.25)., Conclusion: The findings indicated that patients in the periodontitis cohort exhibited a higher risk of developing oral cancer than those in the gingivitis cohort.

Background and Objective: Volatile sulfur compounds may be the main source of oral malodor. The aim of this study was to clarify the relationship between periodontal parameters and volatile sulfur compounds and to evaluate the improvement of several halitosis-related outcomes by tongue scraping, nonsurgical periodontal treatment (including oral hygiene instruction) and oral hygiene instruction/chlorhexidine + cetyl pyridinium gargling., Material and Methods: Seventy-two chronic periodontitis patients with heavy tongue coating were assessed for oral malodor and periodontal status. Oral malodor was evaluated by measuring the levels of volatile sulfur compounds using OralChroma and the organoleptic test score. Thirty participants were selected for the subsequent experiments: tongue scraping; nonsurgical periodontal treatment; and oral hygiene instruction/chlorhexidine + cetyl pyridinium gargling. Twenty-five participants completed all experimental stages., Results: Significant correlations were observed between the organoleptic test score and hydrogen sulfide (H2S), methyl mercapton (CH3SH), tongue coating score and volatile sulfur compounds, which was also significantly correlated with bleeding on probing percentage and tongue coating score. Tongue scraping significantly reduced the levels of volatile sulfur compounds. Further reduction of volatile sulfur compounds after nonsurgical periodontal treatment and oral hygiene instruction/chlorhexidine + cetyl pyridinium gargling were noted compared with baseline., Conclusion: Volatile sulfur compounds, with H2S and CH3SH as the main components, in mouth air are the prominent elements of malodor. Volatile sulfur compounds were decreased by more than 50% after tongue scraping. Nonsurgical periodontal treatment and oral hygiene instruction/chlorhexidine + cetyl pyridinium gargling maintained a significantly lower level of malodor compared with baseline.

Objectives: Reactive oxygen species (ROS) are implicated in the destruction of the periodontium during inflammatory periodontal diseases. The imbalance in oxidant/antioxidant activity may be a key factor in the damaging effects of ROS. This study aimed to determine the lipid peroxidation levels in gingival crevicular fluid and saliva, and glutathione (GSH) and glutathione peroxidase (GPx) in saliva in patients with chronic periodontitis., Methods: Gingival crevicular fluid and saliva were collected from 13 patients and 9 healthy control subjects during the preliminary study, and from 21 patients during the subsequent study. Lipid peroxidation level, GSH level and GPx activity were determined by spectrophotometric assay., Results: The preliminary study found that when comparing patients to healthy controls, the gingival crevicular fluid samples produced the following results, respectively: higher lipid peroxidation concentration (microm) (by sites: 167.55 vs. 53.71, p < 0.0001; by subjects: 151.99 vs. 50.66, p < 0.005) and total amount (pmol) (by sites: 93.02 vs. 8.47, p < 0.0001, by subjects: 80.44 vs. 7.84, p < 0.0005). In saliva samples, lower GSH concentration (microm) (373.04 vs. 606.67, p < 0.05), higher lipid peroxidation concentration (microm) (0.66 vs. 0.13, p < 0.0005), and no difference in GPx activity were found in patients than in those of healthy controls. The subsequent study showed statistically significant (p < 0.05) improvement of clinical periodontal parameters (plaque index, gingival index, probing attachment level, probing pocket depth and gingival crevicular fluid volume), decreases in gingival crevicular fluid lipid peroxidation levels (concentration and total amount) at the sites after the completion of phase 1 periodontal treatment. Similarly, the periodontal treatment resulted in a significant decrease of lipid peroxidation concentrations (p < 0.05), increase in GSH concentration (p < 0.001), and no change in GPx activity in saliva samples., Conclusion: The increased levels of lipid peroxidation may play a role in the inflammation and destruction of the periodontium in periodontitis.

Objectives: To determine differences in radiographic alveolar bone loss (RABL) by age group, gender and tooth type in subjects with adult periodontitis using the digital scanning radiographic image analysis (DSRIA) method., Methods: A total of 4262 teeth were examined for RABL in 178 individuals (96 males and 82 females). Mesial and distal sites were determined by the DSRIA method following scanning of periapical radiographs and using the Microstation 95 image software., Results: Linear assessment of RABL using DSRIA revealed the following results. Mean bone loss of maxillary and mandibular anterior teeth was significantly higher (P<0.001 and P<0.01, respectively) in males compared with females using a two-sample t-test. The highest values of mean RABL occurred most commonly in the maxillary first molars (53.8% and 51.4% for females and males, respectively) and the mandibular central incisors (50.4% and 41.5% for males and females, respectively). Mean RABL was greater in males than in females for both the mandibular and maxillary arches, with the exception of molar sites., Conclusions: Maxillary first molars and mandibular incisors are the highest risk sites. Moreover, greater loss occurs at the molar site in females compared with males for untreated periodontitis in Taiwan Chinese people.

Objective: We investigated the association between glycemic control of type 2 diabetes mellitus (type 2 DM) and severe periodontal disease in the US adult population ages 45 years and older., Methods: Data on 4343 persons ages 45-90 years from the National Health and Nutrition Examination Study III were analyzed using weighted multivariable logistic regression. Severe periodontal disease was defined as 2 + sites with 6 + mm loss of attachment and at least one site with probing pocket depth of 5 + mm. Individuals with fasting plasma glucose > 126 mg/dL were classified as having diabetes; those with poorly controlled diabetes (PCDM) had glycosylated hemoglobin > 9% and those with better-controlled diabetes (BCDM) had glycosylated hemoglobin

TGF-beta 1 is a multifunctional molecule which has unique and potent effects on many target cells and tissues. TGF-beta 1 may promote inflammatory reaction by certain intercellular interaction. TGF-beta 1 at extremely low concentrations shows strong chemotatic activity for mononuclear phagocytes and stimulates bone resorption by enhancing production of PGE2. On the other hand, TGF-beta 1 plays a very important role in the regulation of extracellular matrix turnover presumably by modulating the action of other growth factors on matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) expression. TGF-beta 1 was identified intra- and extracellularly in the inflamed gingival tissues and the distribution was associated with areas of inflammation. Sixteen miniature swines were used in this experimental gingivitis/periodontitis study. The ligatures were placed in situ for periods of 3, 5, 8 and 13 weeks and peroral innoculations of Porphyromonas gingivalis/Actinomyces viscosus into the ligatures were carried out only in the experimental group. ELISA was used to measure the levels of TGF-beta 1 in gingival tissues from the experimental and control groups. Recording of the clinical periodontal parameters was performed and the proportion of black-pigmented Bacteroides in the ligature (plaques) removed immediately prior to the biopsies was recorded. The results revealed that the concentration of TGF-beta 1 of the experimental group was higher and significantly different in statistics on the period of third week than that of the control group. The concentration of TGF-beta 1 was significantly different between the third week and the thirteenth week in the experimental group, and was negatively related to the time-length of ligatures. Furthermore, the concentration of TGF-beta 1 was negatively related to the changes of the calculus index and gingival index. These data indicated that the concentration of TGF-beta 1 of gingival tissue exhibited dynamic changes associated with the progression of experimental periodontal inflammation. The levels of TGF-beta 1 in gingival tissue may be valuable in detecting the inflammatory reaction of periodontal tissues.

This report describes a significant bone regeneration in a mandibular molar with advancing long-standing periodontal disease (defect extending to apex and into furcation) following a single episode of scaling and root planing. A 52-year-old female suffered from generalized moderate periodontitis for two years. An acute periodontal abscess with a 12 mm probing depth around the right mandibular first molar was noted. After incision and drainage, thorough scaling and root planing was performed under local anaesthesia. Three months later, radiographic examination showed complete bone regeneration with formation of a distinct lamina dura. It was concluded that favorable clinical and radiographic results could be obtained after a single episode of thorough subgingival root planing combined with excellent oral hygiene maintenance.

The present study was designed to determine in a cross-sectional study whether there was any relationship between the levels of lactoferrin in gingival crevicular fluid and clinical periodontal parameters. Crevicular fluid was collected from individual sites using standardized filter paper strips (clinically healthy sites, N = 23; periodontitis sites, n = 66) and evaluated for lactoferrin by enzyme-linked immunosorbent assay. The data showed that: (1) the total amounts of lactoferrin were 0.003-0.021 ng (30 second sample) (average 0.009 +/- 0.005 ng) in a clinically healthy periodontium group and 0.016-3.847 ng (30 second sample) (average 0.575 +/- 0.069 ng) in adult periodontitis patients (statistically significantly higher in adult periodontitis patients); and (2) the total amounts of lactoferrin were significantly correlated with clinical parameters, especially a strong positive correlation with gingival crevicular fluid volume (r = 0.85, p < 0.01) and with probing depth (r = 0.71, p < 0.01). These results indicated that quantification of lactoferrin in gingival crevicular fluid may be a more sensitive indicator of periodontal pathology than traditional clinical indices.

The purposes of this study were to investigate the furcation entrance angle (FEA) and the distance between cemento-enamel junction (CEJ) and furcation entrance (FE) of the extracted maxillary and mandibular molars. Assay teeth comprised 89 maxillary molars and 93 mandibular molars. All the FEAs and CEJ-FEs of the molars were measured by a stereomicroscope at 2.5 x equipped with a Bioscan OPTIMAS Image Analyzer (BOIA). The results were summarized as follows: (1) The mean FEAs in the buccal, mesial and distal furcations were 96.3 +/- 10.0, 103.8 +/- 9.7, and 107.2 +/- 12.2 degrees in the maxillary molars, and 91.6 +/- 11.7, 101.7 +/- 11.5, and 97.1 +/- 10.7 degrees in the maxillary second molars, respectively. At the buccal and lingual furcations of mandibular first and second molars, they measured 100.5 +/- 9.7/102.7 +/- 8.5, and 93.3 +/- 11.5/91.7 +/- 10.8 degrees, respectively. (2) The mean distance of CEJ-FEs at the buccal, mesial and distal furcations of maxillary molars were 3.42 +/- 1.5mm, 3.55 +/- 0.97 mm, and 3.69 +/- 0.98mm for the first molars, and 3.01 +/- 1.04mm, 4.04 +/- 1.58mm and 3.00 +/- 1.14mm for the second molars. At the buccal and lingual furcations of the mandibular first and second molars, they were recorded as 1.90 +/- 0.08mm and 2.90 +/- 0.07mm, and 2.82 +/- 1.34mm and 3.46 +/- 1.03mm, respectively. It was concluded that buccal FEA of maxillary 2nd molar was the smallest (91.56 +/- 9.68 degrees) as compared to the mesial and distal FEAs; whereas the mean distance of CEJ-FEs at the buccal surface was the smallest (1.90mm +/- 0.08mm) when compared to the others.

In order to understand the role of IL-1 beta and IL-6 in the periodontal tissue destruction coincident to periodontitis, we assessed the levels of these two mediators in both the gingival tissue and the serum of patients with periodontal disease and of periodontally healthy subjects. In addition, production of IL-6 by six healthy human gingival fibroblast (HGF) strains in response to IL-1 beta was also investigated. The levels of IL-1 beta and IL-6 in gingival tissues and in serum were examined by ELISA. Both mediators were observed to increase in diseased tissues of patients with adult periodontitis, and there was a positively significant relationship between both mediators and clinical assessments of periodontal destruction. Moreover, a significant correlation was also noted between levels of IL-1 beta and IL-6 in gingival tissues of periodontitis patients (r = 0.4334, p < 0.01). However, there was no significant difference in the serum levels of IL-1 beta and IL-6 between periodontitis patients and periodontally healthy controls. In fibroblast cultures, confluent monolayers of HGF were incubated with recombinant human IL-1 beta for 48 h at 37 degrees C in 5% CO2 and air. At the end of the culture period, supernatants were collected and assayed for IL-6 activity by inducing proliferation in the IL-6-dependent hybridoma cell line 7TD1. A dose-dependent stimulatory effect of IL-1 beta on IL-6 production by HGF was noted, wherein 3 strains exhibited higher IL-6 activity than the other 3. These data indicate that the levels of IL-1 beta and IL-6 in gingival tissues are closely related to the severity of periodontal disease and that the IL-1 beta and IL-6 produced in gingival tissues may not reflect these two mediators levels in serum. Moreover, IL-1 beta responsiveness of HGF in IL-6 production depends on both the concentration of IL-1 beta and cells of individual subjects. Since HGF are present in periodontal lesion, it is possible that IL-6 secretion stimulated by exposure to inflammatory cell products such as IL-1 beta may participate in the destruction of periodontal tissue in periodontitis.

The crown and sleeve-coping (CSC) telescope denture is a removable prosthesis that is supported by both selectively retained teeth and the residual ridge or mucosa. Limited information regarding longitudinal studies of the CSC telescope denture has been reported as to the response of the abutments and their surrounding periodontal tissues to this type of design. The authors have documented a longitudinal ten-year follow-up of a case which was considered 'hopeless' for oral rehabilitation because of advanced periodontitis. The CSC telescope denture used in this case resulted in a significant improvement to the remaining dentition. The beneficial results of this form of treatment can be considered for a wide variety of clinical applications for the severely advanced periodontitis case.

We investigated the relationship between molar root fusion and localized periodontitis in this study. A total of 143 individuals (1,109 molars) aged 23 to 68 years were examined for the presence of molar root fusion at diseased and healthy sites. Molar root fusions were diagnosed by periapical radiographs and clinical probing. Periodontal parameters measured included probing depth (PD), clinical attachment loss (CAL), gingival index (GI), and plaque index (PLI) around fused molars. Results indicated that the prevalence of molar root fusions in males and females was 15.2% (93/612) and 32.2% (160/497), respectively. The distribution of molars with root fusions occurs in the following order: maxillary second molars (51.8%), mandibular second molars (32.3%), maxillary first molars (5.7%), and mandibular first molars (0%). Statistically significant differences were observed between molar root fusions at healthy and diseased sites with respect to PLI, GI, PD, and CAL. The highest prevalence of molar root fusion was observed in females.

The objective of the present study was to evaluate the long-term effectiveness of clinical trials of ultrasonic scaling performed solely by a periodontist. A total of 51 individuals (27 males and 24 females) ranging in age from 21 to 61 years with moderate to advanced periodontitis were investigated following baseline assessments included gingival index (GI), plaque index (PlI), probing pocket depths (PPDs), and probing attachment levels (PALs). The individuals were subjected to active supra- and subgingival ultrasonic scaling by a periodontist alone following meticulous oral hygiene instruction. The results revealed a significant (p < 0.001) reduction of mean GI and PlI scores. In addition, a significant and sustained reduction of mean PPDs (p < 0.001) as well as significant sustained gain of mean PALs (p < 0.001) with initial PPDs of 4-6 mm and > or = 7 were greater than those sites with initial PPDs of 1-3 mm at each time interval. Basically, there exists a greater reduction of mean PPDs and greater gain of mean PALs on the buccal and lingual sites than those on the mesial and distal sites at each time interval.

The purpose of the present study was to document the mean proximal alveolar bone loss of molars. The samples consisted of 219 subjects receiving of full mouth radiographs by standardized paralleling technique from Jan, 1992 to Jun, 1994. All the radiographs of 219 individuals suffered from adult periodontitis at age between 20 and 65 years old were measured, and were assessed mean proximal alveolar bone loss of molars and associated contributing factors. The main results indicated that (1) the mean proximal alveolar bone loss of the maxillary first and second molars accounted for 38. 4% and 33.5%, respectively, whereas the mandibular first and second molars were 34.8% and 31.6%, respectively; (2) within the same dental arch, mean proximal alveolar bone loss of the first molars was significant greater than that of the second molars, while the bone loss in the maxillary first molars was significant greater than that of the mandibular first molars. There was no difference between mean proximal bone loss of the maxillary and mandibular second molars; (3) mean alveolar bone loss of the first molars was significant greater than second molars in the same side of the dental arch. There was no significant difference in the mean proximal alveolar bone loss between right and left side molars. (4) average bone loss was the greatest (39.4%) at the mesial surfaces of maxillary first molars, whereas the least mean alveolar bone loss appeared at the distal surfaces of mandibular second molars. A significant difference of mean proximal alveolar bone loss was found between mesial and distal surfaces in mandibular first molars.

The purposes of the study were as follows: (1) to evaluate the molar furcation involvement and number of molar correlated with age and sex; and (2) to study the relationship between the means of alveolar bone loss and associated factors of molar furcation involvements (FIs). 1102 molars (703 males and 399 females) were measured in 219 individuals (136 males and 83 females) for the alveolar bone loss and associated factors of molar furcation involvements. Based on the results, we conclude the following: (1) the higher prevalence of FI was in the mandibular first molar (94.6%), whereas the lowest prevalence of FI was in maxillary second molar; (2) except for the mandibular first molar, the prevalence of molar FI markedly increased with an increased age group (16 & 26, r = 0.335, p < 0.01; 17 & 27, r = 0.345, p < 0.01; 37 & 47, r = 0.239, p < 0.01); (3) the prevalence of molar FI was significantly higher in males than in females (p < 0.05); (4) the mean number of molar FI was significant greater in males (mean = 3.45) than in females (mean = 2.69); (5) factors such as age (r = 0.222, p < 0.01), sex, (r = 0.145, p < 0.05), number of remaining teeth (r = -0.330, p < 0.01) and molar FI (r = 0.471, p < 0.01) are strongly associated with the mean alveolar bone loss of molars.

The purpose of the present study was to examine and evaluate the effect of clinical trials of non-surgical periodontal therapy (NSPT) by ultrasonic scaling alone for three years. A total of 51 individuals (27 males; 24 females) ranging in age from 21 to 61 years with moderately to extremely advanced periodontitis were studied following baseline assessments which included gingival index, plaque index, probing pocket depths, and probing attachment levels (PALs). The patients were subjected to NSPT by using supra- and subgingival scaling with ultrasonic instrumentation alone. The results showed that this therapy resulted in a pronounced and significant reduction (p < 0.001) of gingival inflammation and dental plaque formation for the 3 years of study. In addition, a significant reduction of probing depth as well as an obvious gain of PALs were found greater in sites with initial depth of 4-6 mm and 7 mm or more (p < 0.001) than those in sites with initial probings of 1-3 mm (p > 0.05) at each survey time point.

Recent in vitro findings indicate that cytokines represent an important pathway of connective tissue destruction in human periodontitis. The biological effects of interleukin-1 beta (IL-1 beta) and interleukin-8 (IL-8) are relevant in this regard, and the objective of this study was to compare the levels of these molecules in gingival crevicular fluids (GCF) from patients with adult periodontitis (experimental group) and from individuals with clinically healthy gingiva (control group). GCF was collected for 30 seconds using a periopaper strip and the volume of the sample determined. Following elution of the fluid, assays for IL-1 beta and IL-8 were carried out by ELISA. The concentrations (ng/ml) of cytokines were calculated in the original volume of GCF on each strip. The total amounts (pg/site) of cytokines were expressed as the concentrations multiplied by volumes of GCF: The total amounts of IL-1 beta and IL-8 of the experimental group were significantly higher than the control group. The total amounts of both cytokines were markedly reduced following phase 1 periodontal treatment. The clinical parameters were positively related to the total amounts of IL-1 beta and IL-8. IL-1 beta concentrations and total amounts were also positively related to IL-8 suggesting that the GCF IL-8 levels are influenced by local IL-1 beta activities. These data indicate that the total amounts of IL-1 beta and IL-8 exhibited dynamic changes upon severity of periodontal disease. The levels of IL-1 beta and IL-8 in GCF are valuable in detecting the inflammation of periodontal tissue.

Supernumerary teeth are relatively common in the maxillary incisor and molar areas. However, bilateral ectopic, fully erupted supernumerary mesiodentes are relatively rare. The present case documents a patient with localized periodontitis of the maxillary first and second molars associated with bilaterally erupted supernumerary teeth located in proximity to the buccal embrasure space between the molars. Combined clinical data suggested that these ectopic mesiodentes predisposed or contributed to the development of localized periodontitis.

A total of 404 maxillary lateral and central incisors were examined in a group of 101 individuals comprising 64 males and 37 females for the presence of palato-radicular groove (PRG). The methods used to document the presence of PRG situated at or apical to the cemento-enamel junction (CEJ) included clinical probing, flap operation and inspection with the aid of an enlarging oral mirror. PRGs were classified by location in the mesial, distal and midpalatal areas of affected teeth. The plaque index (P1I), gingival index (GI) and probing pocket depth (PPD) were recorded on the lingual aspect of the teeth examined. Those PRG with initial PPDs of > or = 4 mm and located at or apical to the CEJ were counted as PRG with PPD. The difference in the PRG location for teeth with and without PPDs was analyzed via the chi 2 test. The relationship between the presence of a PRG and the patients periodontal health and plaque accumulation were analyzed using the t-test.(ABSTRACT TRUNCATED AT 250 WORDS)

In the present study we identified a gram-negative anaerobic rod referred to as Y4 which was cytotoxic for human polymorphonuclear leukocytes. Y4 was isolated from dental plaque of a patient with juvenile periodontitis and presented most of the taxonomic characteristics of Actinobacillus species. Under experimental conditions, viable Y4 were cytotoxic for human peripheral blood polymorphonuclear leukocytes in serum-free cultures. Cytotoxicity was dependent on bacterial concentrations and was enhanced in the presence of a fresh or heat-inactivated (56 degrees C, 30 min) autologous serum. Leukotoxicity was independent of phagocytosis. Y4 leukotoxic effect was abolished when bacteria were heat treated (56 degrees C, 30 min) or when incubations were carried out at 4 degrees C instead of at 37 degrees C. The leukotoxicity was monitored by electron microscopy and biochemically by measuring lactate dehydrogenase indicator of cell viability. No cytotoxic effects of Y4 on human mononuclear cells, chicken fibroblasts, or mouse macrophages were detected under the conditions studied. Polymorphonuclear leukocytes may play an important role in the host defense against bacteria in periodontal disease. The cytotoxic effect of Y4 for polymorphonuclear leukocytes presented in this study is the first report of a direct offensive microbial vector in a plaque-derived microorganism and may prove to be relevant in the pathogenesis of juvenile periodontitis.

A relatively high incidence of infection by Actinobacillus actionomycetemcomitans can be shown in subgingival plaque samples obtained from patients with juvenile periodontitis. These organisms possess a potent leukotoxin(s) which rapidly destroys isolated human polymorphonuclear leukocytes (PMNs) and monocytes. If such leukotoxins operate in vivo, they could deprive the gingival crevice area of an essential antibacterial defense mechanism. We have found that sera from juvenile periodontitis patients consistently (greater than 90%) contain antibodies which neutralize Actinobacillus actinomycetemcomitans leukotoxin(s). On the other hand, sera from normal individuals or patients with other types of periodontal disease usually amplified rather than inhibited the leukotoxic reaction. Many patients with juvenile periodontitis have demonstrable defects in PMN or monocyte chemotaxis and this may place them at risk to gingival infection by Actinobacillus actinomycetemcomitans. The immune response against these organisms could be a crucial determinant in the course of juvenile periodontitis. While this disease is relatively rare, it does cause immeasurable emotional, physical and economic hardship for patients and their families. The identification of Actinobacillus actinomycetemcomitans as a potential pathogen in this disorder may eventually lead to specific forms of therapy to prevent and eliminate infection by this organism in these patients.

The purpose of this study was to examine and evaluate the short-term (six months) effects of clinical trials of nonsurgical periodontal therapy. The subjects studied included consisted of 34 patients, 24-52 years of age (836 teeth), with various degrees of advanced periodontitis. Following a baseline examination which included assessments of the gingival index (GI), plaque index (PlI), calculus index (CI), probing depth, and attachment level, the patients were subjected to nonsurgical therapy. Differences between various treatment intervals for the pockets initially measuring 1-3 mm, 4-6 mm, and 7 mm or more were analyzed by using the paired Students t-test. Following meticulous debridement of periodontal pockets with ultrasonic instrumentation, routine pocket irrigation with hydrogen peroxide (2.5-3.0%) and chlorhexidine gluconate solutions (0.12%) was performed by the authors as well as by the patients at sites with moderate to deep pockets and furcation involvement. Furthermore, the patients were supervised under a maintenance care program which provided patient motivation, the teaching of oral hygiene procedures, and offered regular recall for six months. The results demonstrated that non-surgical therapy resulted in a prominent reduction of gingival inflammation, dental plaque and calculus formation, and finally increased gingival recession. Also, for sites with an initial probing depth of 1-3 mm, there was a slight loss (0.1 mm) of the attachment level, 3 and 6 months after therapy. For sites with an initial probing depth of 4-6 mm, there was some attachment gain (0.31 mm and 0.69 mm) at 3 and 6 month post-treatment intervals. For pockets 7 mm or more in depth, a pronounced gain (0.49 mm and 1.00 mm) of attachment was noted following 3 and 6 month intervals. Generally, an obvious reduction of probing depth was constantly observed after nonsurgical treatment in each of the three initial pocket groups mentioned above. The changes of probing depths between baseline and at 3 or 6 months after treatment were 0.17 and 0.23, 1.23 and 1.75, and 1.83 and 2.63 mm, respectively. With the exception of attachment loss for the pockets initially measuring 1-3 mm, the difference of GI, PlI, CI, probing depth, and attachment level between baseline and 3 or 6 months after treatment were found statistically significant in each of the three initial pocket groups when analyzed individually by ANOVA.

Background and Objective Periodontitis is a highly prevalent chronic inflammatory disease that causes tooth loss, morbidity and confers an increased risk for systemic disease. Tissue destruction during periodontitis is due in large part to collagen-degrading matrix metalloproteinases ( MMPs) released by resident cells of the periodontium in response to proinflammatory cytokines. Platelets are immune-competent blood cells with a newly recognized role in chronic inflammation; however, their role in the pathogenesis of periodontitis is undefined. Consequently, the objective of this study was to assess the effect of platelet factor 4 ( PF4), a major platelet-derived cytokine, on MMP-1 (collagenase) expression in human gingival fibroblasts ( HGFs). Material and Methods HGFs were cultured in the presence or absence of recombinant PF4. Pro- MMP-1 secretion was quantified by enzyme-linked immunosorbent assay analysis of the cell culture supernatants. MMP-1 transcription was quantified by real-time polymerase chain reaction. Regulation of MMP-1 production by the p44/42 MAP kinase ( MAPK) signaling pathway was examined in the presence or absence of PF4. Results Exposure to PF4 caused a ~ 2-3-fold increase in MMP-1 transcription and secretion from cultured HGFs. PF4 treatment also enhanced phosphorylation of p44/42 MAPK, which has been previously shown to induce MMP-1 expression in fibroblasts. Blockade of p44/42 MAPK signaling with the cell-permeant inhibitors PD98059 and PD184352 abrogated PF4-induced pro- MMP-1 transcription upregulation and release from cultured HGFs. Conclusion We conclude that PF4 upregulates MMP-1 expression in HGFs in a p44/42 MAPK-dependent manner. These findings point to a previously unidentified role for platelets in the pathogenesis of periodontal diseases. [ABSTRACT FROM AUTHOR]

Background and Objective The present study investigated the association between the RAGE G82S polymorphism, the plasma levels of sRAGE and chronic periodontitis in subjects with and without diabetes mellitus ( DM). Material and Methods A total of 230 patients with DM and 264 non- DM participants were recruited for this study. Genotyping of the RAGE G82S polymorphism was accomplished using polymerase chain reaction-restriction fragment length polymorphism, and associations were analyzed with the chi-squared test and logistic regression analysis. Results In the non- DM group, the chi-squared test showed that the frequency distributions of the G82S polymorphism were significantly different between chronic periodontitis and non- chronic periodontitis subjects (χ2 = 8.39, p = 0.02). A multivariate logistic regression model showed that the (G82S + S82S) genotypes were associated with a significantly increased risk of chronic periodontitis development compared to the G82G genotype (adjusted odds ratio = 2.06, 95% confidence interval: 1.08-4.07). In the DM group, there was no association between the G82S polymorphism and chronic periodontitis development when a multivariate logistic regression was performed. Plasma levels of sRAGE were significantly higher in subjects with the G82G genotype compared to those with the (G82S + S82S) genotypes in both the non- DM (856.6 ± 332.0 vs. 720.4 ± 311.4 pg/ mL, p = 0.003) and DM groups (915.3 ± 497.1 vs. 603.5 ± 298.3 pg/ mL, p < 0.0001). However, there was no difference in plasma sRAGE levels between chronic periodontitis and non- chronic periodontitis subjects in both the DM and non- DM groups. Moreover, when the subjects were further sub-divided by the G82S polymorphism, the difference in plasma levels of sRAGE between chronic periodontitis and non- chronic periodontitis subjects in the DM and non- DM groups remained statistically insignificant. Conclusions The present study revealed that the RAGE G82S polymorphism was associated with chronic periodontitis in the non- DM group but not in the DM group. Our results also showed that the plasma levels of sRAGE were significantly higher in subjects with the RAGE G82G genotype, and this correlation was not affected by the presence of chronic periodontitis in the DM and non- DM groups. [ABSTRACT FROM AUTHOR]

Aim: Periodontal disease encompasses gingivitis and periodontitis, which exerts systemic effects. We conducted a population-based study to evaluate the association between periodontal disease and the risk of cancer.Methods: We used insurance claims data from 1997 to 2010, accessing a database of 1 million randomly selected insurants in Taiwan. All patients were older than 20 and newly diagnosed with periodontitis between 1 January 1997 and 31 December 2010. The comparison cohort comprised patients older than 20, who were newly diagnosed with gingivitis in the same period. Both cohorts were followed until a cancer diagnosis, lost to follow-up, death, termination of insurance, or the end of 2010.Results: The incidence rate of cancer was 1.14 times higher in the study cohort than in the comparison cohort [confidence interval (CI) = 1.11–1.17]. The adjusted hazard ratio (HR) was 1.05 (95% CI = 1.00–1.11). A multivariable analysis showed that the periodontitis patients exhibited an elevated risk of developing oral cancer (adjusted HR = 1.79, 95% CI = 1.42–2.25).Conclusion: The findings indicated that patients in the periodontitis cohort exhibited a higher risk of developing oral cancer than those in the gingivitis cohort. [ABSTRACT FROM PUBLISHER]

Wu Y-M, Chuang H-L, Ho Y-P, Ho K-Y, Tsai C-C. Investigation of interleukin-13 gene polymorphisms in individuals with chronic and generalized aggressive periodontitis in a Taiwanese (Chinese) population. J Periodont Res 2010; 45: 695–701. © 2010 John Wiley & Sons A/S Background and Objective: The interleukin-13 (IL-13) −1112 C/T polymorphisms have been analyzed previously in a North European population of patients with aggressive periodontitis. The present study was carried out to investigate the association of polymorphisms in the IL-13 gene with susceptibility to periodontitis in a Taiwanese population. Material and Methods: The genotyping of IL-13 −1112 C/T polymorphisms in 60 patients with aggressive periodontitis, 204 patients with chronic periodontitis and 95 healthy controls was carried out using the polymerase chain reaction–restriction fragment length polymorphism technique. Genotypes and allele frequencies among study groups were compared using Fisher’s exact test ( p < 0.05). Pearson’s chi-square test was used for analysis of the Hardy–Weinberg equilibrium. Results: The distributions of CC genotypes and C alleles between patients with aggressive periodontitis and healthy controls were significantly different ( p = 0.034 and 0.046). After adjustment for age, gender, betel nut chewing and smoking status using logistic regression analysis, the odds ratio (OR) was 6.45 [95% confidence interval (CI) = 1.99–23.72, p = 0.003] for aggressive periodontitis. However, the CC genotype was only significantly associated with the risk of aggressive periodontitis in the nonsmoking group (OR = 4.48, 95% CI = 1.31–16.93, p = 0.020). Conclusion: The CC genotype or C allele appears to increase the risk of developing aggressive periodontitis in Taiwanese subjects. [ABSTRACT FROM AUTHOR]

Background and Objective: A dramatic difference in the frequencies of the Lys/Arg single nucleotide polymorphism in the lactoferrin genotype between a small population of patients with localized juvenile periodontitis and healthy subjects has been reported. As the single nucleotide polymorphism could be associated with ethnicity, the present study aimed to investigate the association between polymorphisms of the lactoferrin gene and periodontitis. Material and Methods: Sixty-five patients with aggressive periodontitis, 278 with chronic periodontitis and 88 healthy controls were genotyped for the Lys/Arg polymorphism of the lactoferrin gene at position 29 [reference sequence (rs) 1126478] in the N-terminal alpha-helical region. Results: The frequencies of the GG genotype and the G allele were highest in the aggressive periodontitis group, followed by the chronic periodontitis group and then the healthy controls. The frequency of the G allele was significantly higher in aggressive periodontitis and chronic periodontitis groups than in healthy controls ( p = 0.0037 and 0.0212). Although the difference of the GG genotype distribution between subjects with chronic periodontitis and healthy controls did not reach significance, the distribution of genotypes between aggressive periodontitis and healthy controls was significantly different. The association of the gene polymorphism and aggressive periodontitis still existed, even after adjusting for age, gender and smoking status by logistic regression analysis (GG/AG+AA: odds ratio = 2.16, 95% confidence interval = 1.09–4.35, p = 0.0287). After the study, subjects were further stratified by their smoking status; the GG genotype was still significantly associated with the risk of aggressive periodontitis in the nonsmoking group (odds ratio = 2.69, p = 0.018). However, there were no statistical differences between chronic periodontitis vs. healthy controls and aggressive periodontitis vs. healthy controls in the smoking group. Conclusion: The present study revealed that the A/G polymorphism in the lactoferrin gene might be associated with aggressive periodontitis. The A allele might reduce the risk of development of aggressive periodontitis in a Taiwanese population. Our results also support the hypothesis that lactoferrin genetic polymorphisms could play a role in the risk for periodontitis separate from the smoking factor. The functionality of this gene’s polymorphisms has to be further elucidated. [ABSTRACT FROM AUTHOR]

Determined differences in radiographic alveolar bone loss by age group, gender and tooth type in subjects with adult periodontitis. Use of digital scanning radiographic image analysis method; Calculation of mean bone loss; Identification of highest risk sites.

A sonic extract of Actinobacillus actinomycetemcomitans Y4, a microorganism originally isolated from a patient with juvenile periodontitis, contains a leukotoxin (Aa-Ieukotoxin) which specifically kills human polymorphonuclear leukocytes (PMNs) and monocytes. In the presence of normal human sera, the toxicity of the leukotoxin is enhanced whereas sera from patients with juvenile periodontitis neutralize leukotoxic activity. In juvenile periodontitis serum immunoglobulin G was identified as the specific inhibitor of the Aaleukotoxin. The leukotoxin enhancing factor(s) in normal human serum appeared to be a large molecular weight protein which was not immunoglobulin. Pooled sera from rabbits immunized with A. actinomycetemcomitans Y4 sonic extract also neutralized Aa- Icukotoxic activity while normal rabbit serum enhanced toxicity. The presence of anti- leukotoxin antibody in sent from individuals with juvenile periodontitis suggests that these people have been immunized with A. actinomycetemcomitans microorganisms. Monitoring of this antibody may be a convenient tool in the study of the etiology of juvenile periodontitis. [ABSTRACT FROM AUTHOR]

An abstract of the article "Cancer Risk Among Gingivitis and Periodontitis Patients: A Nationwide Cohort Study" by B. W. Wen, C. S. Tsai, C. L. Lin, et al. that appeared in a 2014 issue of "QJM: An International Journal of Medicine" is presented.