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Background and Objective: Attachment loss of the junctional epithelium and alveolar bone destruction are signs of periodontitis, which is mainly caused by an inflammatory response to dental plaque. Glycyrrhetinic acid (GA), a component of the licorice herb, has been shown to have important anti-inflammatory activities; however, there are no previous reports on the ability of its inhibitory effects to prevent periodontal diseases. Hence, in this study, using our experimental periodontitis model, we attempted to evaluate whether GA had an effect on the prevention of attachment loss and alveolar bone loss., Material and Methods: Rats were intraperitoneally immunized with Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 5) received 3 topical applications of 50 μg/μL of LPS followed by one application of the vehicle (propylene glycol:ethyl alcohol:phosphate-buffered saline [PBS] = 8:1:1) into the gingival sulcus. This protocol was repeated twice per day for 10 days. The low (n = 5) and high (n = 5) groups received topical application of LPS and 0.03% or 0.3% GA, respectively. The control group received topical application of PBS and vehicle. The rats were killed on the 10th day. Attachment loss, alveolar bone level and inflammatory cell infiltration were investigated histometrically. The formation of immune complexes and infiltration of LPS were evaluated immunohistologically., Results: Attachment loss, formation of immune complexes and infiltration of inflammatory cells were increased in the LPS group compared with the control group, and were completely inhibited in the low and high groups compared with the LPS group. The LPS group showed greater alveolar bone destruction compared with the control group and GA-treated groups. In addition, invasion of LPS was detected in the LPS group, was absent in the control group and was weaker in the GA-treated groups than in the LPS group., Conclusion: In the present study, we showed that GA inhibits periodontal destruction in the rat experimental periodontitis model., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Objective: The aim of the present study was to compare clinical periodontal parameters and to assess the release of C-telopeptides pyridinoline cross-links (ICTP) and C-terminal crosslinked telopeptide (CTX) from gingival collagen of naswar (NW) and non-naswar (control) dippers., Material and Methods: Eighty-seven individuals (42 individuals consuming NW and 45 controls) were included. Clinical (plaque index, bleeding on probing, probing depth and clinical attachment loss) and radiographic (marginal bone loss) periodontal parameters were compared among NW and control groups. Gingival specimens were taken from subjects in NW and control groups, assessed for ICTP and CTX levels (using ELISA) and analyzed using micro-Raman spectroscopy. The significance of differences in periodontal parameters between the groups was determined using Kruskal-Wallis and Mann-Whitney U tests. The percent loss of dry mass over exposure time and the rate of release of ICTP and CTX from all groups were compared using the paired t-test to examine the effects of exposure time., Results: Clinical and radiographic periodontal parameters were significantly higher in the NW group than the control group (P < .01). In the Raman spectrum, the strongest and sharpest band occurred at 1260 cm -1 amongst NW users. A Raman band at Amide I was observed with slight shifts in wave numbers. The rate of ICTP and CTX release was significantly higher in subjects from the NW group compared with those from the control group (P < .05). Both factors, the type of groups and time, had a significant effect on release of ICTP and CTX (P < .05)., Conclusion: Within the limits of the present study, it may be concluded that clinical and radiographic periodontal parameters were worse among subjects in the NW group than in those of the control group. There is a higher degree of collagen breakdown in the connective tissue of subjects in the NW group as a result of naswar usage., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Objective: Perforated barrier membranes open channels between the suprabony and intrabony compartments of the defect, which could allow for more physiologic cellular interactions between different components of the periodontium during guided tissue regeneration surgery. To test this assumption, this study was designed to evaluate levels of vascular endothelial cell growth factor (VEGF) and platelet-derived growth factor (PDGF)-BB in gingival crevicular fluid during the early stages of healing of localized intrabony defects treated with perforated membranes (PMs) or non-PMs, as compared with open flap debridement., Material and Methods: Thirty non-smoking patients with severe chronic periodontitis participated in this prospective, randomized and single blinded trial. Each patient contributed one interproximal defect that was randomly assigned to the PM group (n = 10), occlusive membrane (OM) group (n = 10) or open flap debridement (OFD) group (n = 10). Plaque index, gingival index, probing depth, clinical attachment level and the intrabony depth of the defect were measured at baseline and reassessed at 6 and 9 mo after therapy. Gingival crevicular fluid samples were collected on days 1, 3, 7, 14, 21 and 30 d after therapy for the changes in VEGF and PDGF-BB levels., Results: During the early stages of healing (1, 3 and 7 d), the mean VEGF and PDGF-BB concentrations at sites treated with PMs and OFD peaked with a statistically significant difference as compared with the OM-treated group. VEGF and PDGF-BB levels at sites treated with PMs and OFD were not statistically different. Growth factor levels decreased sharply in the samples obtained at days 21 and 30 with non-significant differences between the three groups. Nine months after therapy, the PM-treated group showed a statistically significant improvement in probing depth, clinical attachment level and intrabony defect compared to the OM and OFD groups., Conclusions: Within the limits of the present study, one can conclude that PM coverage of periodontal defects is associated with initial gingival crevicular fluid growth factor upregulation that could improve the clinical outcomes of guided tissue regeneration surgery., (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Objective: Insufficient information on the cellular composition of long-standing gingivitis lesions without signs of attachment loss makes an understanding of differences in cellular composition between "destructive" and "nondestructive" periodontal lesions difficult. The aim of the current study was to analyze differences in cell characteristics between lesions representing long-standing gingivitis and severe periodontitis., Material and Methods: Two groups of patients were recruited. One group consisted of 36 patients, 33-67 years of age, with severe generalized periodontitis (periodontitis group). The second group consisted of 28 patients, 41-70 years of age, with overt signs of gingival inflammation but no attachment loss (gingivitis group). From each patient a gingival biopsy was obtained from one selected diseased site and prepared for immunohistochemical analysis., Results: Periodontitis lesions were twice as large and contained significantly larger proportions, numbers and densities of cells positive for CD138 (plasma cells) and CD68 (macrophages) than did gingivitis lesions. The proportion of B cells that expressed the additional CD5 marker (B-1a cells) was significantly larger in periodontitis lesions than in gingivitis lesions. The densities of T cells and B cells did not differ between periodontitis lesions and gingivitis lesions. T cells were not the dominating cell type in gingivitis lesions, as B cells together with their subset plasma cells comprised a larger number and proportion than T cells., Conclusion: Periodontitis lesions at teeth with advanced attachment and bone loss exhibit quantitative and qualitative differences in relation to gingivitis lesions at teeth with no attachment and bone loss. It is suggested that the large number and high density of plasma cells are the hallmarks of advanced periodontitis lesions and the most conspicuous difference in relation to long-standing gingivitis lesions., (© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Objective: Green tea extract exerts a variety of biological effects, including anti-inflammatory activities. However, there has been no report on the effect of green tea extract on loss of attachment, which is an important characteristic of periodontitis. Here, we examined the inhibitory effects of green tea extract on the onset of periodontitis in a rat model., Material and Methods: Rats were immunized intraperitoneally with Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 12) received a topical application of LPS onto the palatal gingival sulcus every 24 h. The green tea extract group (n = 12) received a topical application of LPS mixed with green tea extract, sunphenon BG, every 24 h. The phosphate-buffered saline (PBS) group (n = 6) received a topical application of PBS every 24 h. The levels of anti-LPS immunoglobulin G (IgG) in serum were determined using ELISA. Rats in the LPS and green tea extract groups were killed after the 10th and 20th applications. Rats in the PBS group were killed after the 20th application. Loss of attachment, level of alveolar bone and inflammatory cell infiltration were investigated histopathologically and histometrically. RANKL-positive cells and the formation of immune complexes were evaluated immunohistologically., Results: There was no significant difference in the serum levels of anti-LPS IgG between the LPS group and the green tea extract group. In contrast, loss of attachment, level of alveolar bone, inflammatory cell infiltration and RANKL expression in the green tea extract group were significantly decreased compared with those in the LPS group., Conclusion: These findings demonstrate that green tea extract suppresses the onset of loss of attachment and alveolar bone resorption in a rat model of experimental periodontitis.

Background and Objective: Occlusal trauma is an important factor that influences the progression of periodontitis, but it is unclear whether occlusal trauma influences periodontal destruction at the onset of periodontitis. We established an experimental periodontitis model with both site-specific loss of attachment and alveolar bone resorption. The purpose of the present study was to investigate the effects of occlusal trauma on periodontal destruction, particularly loss of attachment, at the onset of experimental periodontitis., Material and Methods: Sixty rats were used in the present study. Forty-eight rats immunized with lipopolysaccharide (LPS) intraperitoneally were divided into four groups. In the trauma (T) group, occlusal trauma was induced by placing an excessively high metal wire in the occlusal surface of the mandibular right first molar. In the inflammation (I) group, periodontal inflammation was induced by topical application of LPS into the palatal gingival sulcus of maxillary right first molars. In the trauma + inflammation (T+I) group, both trauma and periodontal inflammation were simultaneously induced. The PBS group was administered phosphate-buffered saline only. Another 12 nonimmunized rats (the n-(T+I) group) were treated as described for the T+I group. All rats were killed after 5 or 10 d, and their maxillary first molars with surrounding tissues were observed histopathologically. Loss of attachment and osteoclasts on the alveolar bone crest were investigated histopathologically. To detect immune complexes, immunohistological staining for C1qB was performed. Collagen fibers were also observed using the picrosirius red-polarization method., Results: There were significant increases in loss of attachment and in the number of osteoclasts in the T+I group compared with the other groups. Moreover, widespread distribution of immune complexes was observed in the T + I group, and collagen fibers oriented from the root surface to the alveolar bone crest had partially disappeared in the T, T+I and n-(T+I) groups., Conclusion: When inflammation was combined with occlusal trauma, immune complexes were confirmed in more expanding areas than in the area of the I group without occlusal trauma, and loss of attachment at the onset of experimental periodontitis was increased. Damage of collagen fibers by occlusal trauma may elevate the permeability of the antigen through the tissue and result in expansion of the area of immune-complex formation and accelerating inflammatory reaction. The periodontal tissue destruction was thus greater in the T+I group than in the I group., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Objective: The effects of tobacco smoking on the prevalence and severity of periodontal disease have been well documented. However, very few studies have assessed the effects of oral smokeless tobacco (ST) on the periodontium. Considering the widespread use of ST products globally, the effects of such products on the periodontal tissues may be important. The present study was performed to compare retrospectively the patterns of periodontal destruction among oral ST users and never-users with periodontitis., Material and Methods: Data from 149 patients with periodontitis (60 ST users and 89 never-users) were compared for mean scores of probing depth, recession (REC) and clinical attachment loss (CAL) and the mean percentage of sites with different ranges of probing depth, REC and CAL., Results: For full-mouth scores, mean REC and CAL were significantly higher in ST users than in never-users (p < 0.001 and p = 0.008, respectively). For different regions of the dentition, mean scores of REC were significantly higher among ST users than among never-users (p < 0.001 for all regions), and mean scores of CAL were significantly higher for ST users in mandibular (p < 0.001), buccal (p = 0.008), lingual (p = 0.022), anterior (p = 0.012) and molar (p = 0.009) sites. Generally, there were higher percentages of sites with shallow pockets (0-3 mm), REC of ≥ 1 mm and CAL of ≥ 3 mm in ST users than in never-users. However, only differences for REC categories were significant for all regions (p < 0.001). ST users had a significantly higher proportion of sites with CAL of ≥8 mm for full-mouth sites (p = 0.003), mandibular teeth (p < 0.001), buccal sites (p = 0.002), anterior teeth (p = 0.040) and molars (p = 0.007)., Conclusion: ST users tend to have more severe REC and CAL and a greater proportion of sites with higher values of REC and CAL compared with never-users. The greatest increase in severity of CAL was found to be localized to sites on mandibular teeth, buccal surfaces, anteriors and molars, which may be a result of the retention of the ST product in the oral cavity., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Objective: Gingival crevicular fluid has been suggested as a possible source of biomarkers for periodontal disease progression. This paper describes a technique for the analysis of gingival crevicular fluid from individual sites using mass spectrometry. It explores the novel use of mass spectrometry to examine the relationship between the relative amounts of proteins and peptides in gingival crevicular fluid and their relationship with clinical indices and periodontal attachment loss in periodontal maintenance patients. The aim of this paper was to assess whether the mass spectrometric analysis of gingival crevicular fluid may allow for the site-specific prediction of periodontal disease progression., Material and Methods: Forty-one periodontal maintenance subjects were followed over 12 mo, with clinical measurements taken at baseline and every 3 mo thereafter. Gingival crevicular fluid was collected from subjects at each visit and was analysed using matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry. Samples were classified based upon pocket depth, modified gingival index (MGI), plaque index and attachment loss, and were analysed within these groups. A genetic algorithm was used to create a model based on pattern analysis to predict sites undergoing attachment loss., Results: Three hundred and eighty-five gingival crevicular fluid samples were analysed. Twenty-five sites under observation in 14 patients exhibited attachment loss of > 2 mm over the 12-mo period. The clinical indices pocket depth, MGI, plaque levels and bleeding on probing served as poor discriminators of gingival crevicular fluid mass spectra. Models generated from the gingival crevicular fluid mass spectra could predict attachment loss at a site with a high specificity (97% recognition capability and 67% cross-validation)., Conclusions: Gingival crevicular fluid mass spectra could be used to predict sites with attachment loss. The use of algorithm-generated models based on gingival crevicular fluid mass spectra may provide utility in the diagnosis of periodontal disease., (© 2012 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Objective: Dentin sialophosphoprotein (DSPP) and its cleaved products, dentin phosphoprotein (DPP) and dentin sialoprotein (DSP), play important roles in biomineralization. Recently, we observed that DSPP is highly expressed in the alveolar bone and cementum, indicating that this molecule may play an important role in the formation and maintenance of a healthy periodontium, and its deletion may cause increased susceptibility to periodontal diseases. The objective of this investigation was to study the effects of Dspp ablation on periodontal tissues by analyzing Dspp null mice., Material and Methods: Newborn to 6-mo-old Dspp null mice were examined, and the 3- and 6-mo-old Dspp null mice were characterized in detail using X-ray radiography, histology and scanning electron microscopy (backscattered as well as resin-infiltrating). Wild-type mice of the same age groups served as the normal controls., Results: The Dspp null mice showed significant loss of alveolar bone and cementum, particularly in the furcation and interproximal regions of the molars. The alveolar bone appeared porous while the quantity of cementum was reduced in the apical region. The canalicular systems and osteocytes in the alveolar bone were abnormal, with reduced numbers of canaliculi and altered osteocyte morphology. The loss of alveolar bone and cementum along with the detachment of the periodontal ligaments (PDL) led to the apical migration of the epithelial attachment and formation of periodontal pockets., Conclusion: Inactivation of DSPP leads to the loss of alveolar bone and cementum and increased susceptibility to bacterial infections in PDL of Dspp null mice. The fact that the loss of DSPP results in periodontal diseases indicates that this molecule plays a vital role in maintaining the health of the periodontium., (© 2012 John Wiley & Sons A/S.)

Background and Objective: The clinical efficacy of EMDs for the treatment of periodontal infrabony defects has been reported. However, recent publications have questioned the validity of results from early findings. Hence, the purpose of this study was to compare the results obtained from early and late studies when EMD was used as an adjunct in treating human intrabony defects during flap surgery. The aim of this meta-analysis was to evaluate the validity of results published from early studies compared with those published from later studies., Material and Methods: PubMed and MEDLINE searches were performed. The evaluation period was 1997-2010 and it was divided into two groups of equal periods of time: early studies (1997-2003) and late studies (2004-2010). The clinical parameters assessed were clinical attachment level (CAL), probing pocket depth and bone gain (BG; measured as a percentage or in mm)., Results: No statistically significant difference was found between the results obtained from early studies (1997-2003) and late studies (2004-2010) with regards to CAL gain, probing pocket depth reduction and BG. Nonetheless, both study periods showed a benefit for using EMD to treat periodontal infrabony defects when compared with the groups without EMD during open flap surgery., Conclusions: The results obtained from this study failed to show any potential differences between the results published from early studies and late studies with regards to the clinical effectiveness of EMD in treating periodontal infrabony defects., (© 2012 John Wiley & Sons A/S.)

Background and Objective:   There are few data concerning the effect of scaling and root planing on the levels of immune and inflammatory mediators in gingival crevicular fluid from patients with chronic periodontitis. Therefore, in this study the influence of scaling and root planing was determined on amounts of interleukin (IL)-1β, IL-8 and MMP-8 in gingival crevicular fluid from patients with chronic periodontitis, in relation to clinical parameters., Material and Methods:   A total of 51 patients were enrolled in this study. The study population consisted of 30 patients with generalized advanced chronic periodontitis, while 21 periodontally healthy subjects were recruited for the control group. The clinical parameters included approximal plaque index, gingival index, pocket depth and clinical attachment loss. The amounts of IL-1β, IL-8 and MMP-8 in gingival crevicular fluid were measured by ELISA. Periodontal parameters as well as gingival crevicular fluid humoral factor amounts were evaluated in the control group and in chronic periodontitis patients at baseline and at 1 and 4 wk after scaling and root planing treatment., Results:   At baseline, there were significant differences between control subjects and chronic periodontitis patients in terms of clinical attachment loss, pocket depth, gingival index (p < 0.001) and approximal plaque index (p < 0.01). The amounts of IL-1β, MMP-8 (p < 0.001) and IL-8 (p < 0.01) in gingival crevicular fluid were significantly lower in healthy subjects than in chronic periodontitis patients. Scaling and root planing led to improvement in all examined clinical parameters, apart from clinical attachment loss. Periodontal treatment also resulted in a significant decrease in the amounts of IL-1β, IL-8 and MMP-8 in comparison to baseline, especially 4 wk after scaling and root planing (p < 0.001); however, the amounts of these humoral factors were still higher than those in control group., Conclusion: Our observations indicated that short-term nonsurgical therapy resulted in a significant improvement in periodontal indices and in a marked decrease of IL-1β, IL-8 and MMP-8 gingival crevicular fluid levels. Nevertheless, no significant correlations were found between clinical parameters and amounts of humoral factors after therapy., (© 2012 John Wiley & Sons A/S.)

Background and Objective: The causes of periodontitis are bacteria and the host immune system, but the role of the immune system in the onset and progression of periodontal disease is still unclear. Our previous report showed that the formation of an immune complex in the gingival sulcus induces periodontal destruction. This study was carried out to investigate how the immune system, particularly immunization, is involved in periodontal destruction., Material and Methods: Animals immunized intraperitoneally with lipopolysaccharide (LPS) were used as the immunized group. The nonimmunized group received only phosphate-buffered saline. LPS was applied daily onto the palatal gingival sulcus in both groups 1 d after the booster injection. Serum levels of anti-LPS IgG were determined. Loss of attachment and the level of alveolar bone were histopathologically and histometrically investigated. RANKL-bearing cells and the expression of C1qB were immunohistologically evaluated., Results: The serum levels of anti-LPS IgG were elevated in the early experimental period in the immunized group. There were significant increases in loss of attachment, level of alveolar bone and the number of RANKL-bearing cells in the immunized group. C1qB was observed in the junctional epithelium and adjacent connective tissue. The nonimmunized group showed similar findings at and after the time when the serum level of anti-LPS IgG was elevated., Conclusion: Topical application of LPS as an antigen induced periodontal destruction when the serum level of anti-LPS IgG was elevated in rats immunized with LPS. The presence of C1qB suggests that the formation of immune complexes is involved in this destruction., (© 2012 John Wiley & Sons A/S.)

Background and Objective: The objective of the present study was to evaluate the expression and the distribution of the transient receptor potential vanilloid receptor 1 (TRPV1) and of toll-like receptor 4 (TLR4) in tissue samples from patients with periodontal disease (aggressive periodontitis and chronic periodontitis) and from healthy controls., Material and Methods: Ten tissue samples from each disease group (aggressive periodontitis and chronic periodontitis) and from healthy subjects were obtained during routine oral surgical procedures. Subgingival specimens were collected from sites with advanced loss of support (probing depth>5mm) and specimens from the corresponding healthy controls were obtained during tooth extraction for orthodontic reasons or following surgical extraction of an impacted third molar. The distribution of TRPV1 and TLR4 receptors in human gingival tissue was studied by immunohistochemistry., Results: Both TLR4 and TRPV1 were detected in gingival tissues from healthy subjects, and from patients with chronic periodontitis and aggressive periodontitis, particularly in gingival keratinocytes, fibroblasts, inflammatory cells and the endothelial lining of capillaries in connective tissues. Histologic examination of the samples from healthy controls disclosed that clinically healthy gingiva does not correspond to histologically healthy gingiva. Subsequently, these samples were redesignated as gingivitis samples. TRPV1 was down-regulated in all cell types in samples obtained from patients with chronic periodontitis compared to samples obtained from patients with gingivitis, whereas TLR4 was down-regulated only in the epithelium and in gingival fibroblasts. In contrast, the levels of these markers in patients with aggressive periodontitis were similar to those in healthy patients., Conclusion: Local expression of TRPV1 and TLR4 in gingival tissues may contribute to both physiological and pathological processes in the periodontium. Our data suggest that TRPV1 and TLR4 may play a role specifically in the pathophysiology of chronic periodontitis., (© 2011 John Wiley & Sons A/S.)

Background and Objective: Host-derived enzymes, cytokines and other proinflammatory mediators play an integral role in periodontal destruction. The levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor-inducible 14 protein (Fn14), are elevated in tissues from a number of chronic inflammatory diseases. The aim of the present study was to investigate the expression of TWEAK and Fn14 at the protein and mRNA levels in gingival biopsies from periodontitis patients and from clinically healthy patients., Materials and Methods: Gingival biopsies were obtained from healthy sites (n = 7) and from sites affected by periodontitis (n = 27). The expression of TWEAK and Fn14 was investigated by immunohistochemistry in formalin-fixed, paraffin-embedded tissues. The levels of mRNA for TWEAK and Fn14 were also investigated by RT-PCR., Results: The expression of TWEAK and Fn14 proteins was significantly higher in periodontitis tissue than in healthy tissue. In periodontitis tissues, TWEAK and Fn14 proteins were mainly expressed by mononuclear leukocytes (morphologically resembling lymphocytes and plasma cells), by cells lining blood vessels, by spindle-shaped cells resembling fibroblasts and by multinucleated cells. The Fn14 mRNA level in periodontitis tissue was significantly higher than that in healthy tissue. A moderate correlation between TWEAK/Fn14 expression and inflammation and bone loss, but not pocket depth, was noted., Conclusion: This study demonstrates higher expression of TWEAK protein and of Fn14 mRNA and protein in periodontitis tissues than in clinically healthy controls. Our data support the concept that TWEAK/Fn14 signaling is an additional player in the pathogenesis of periodontitis and adds to the increasing number of cytokine networks involved in periodontal inflammation.

Background and Objective: Limited information is available on the expression and distribution of syndecan-1 within human gingival tissues/cells and on putative factors that might affect its expression. Therefore, the objective of the present study was to determine immunohistochemically the expression and distribution of syndecan-1 in the gingival tissues of patients with chronic periodontitis and to examine the correlation of syndecan-1 expression with various putative factors (environmental, patient/systemic and local factors)., Material and Methods: Gingival specimens were surgically excised from the area of the junctional/pocket epithelium (study group 1, including 30 chronic periodontitis patients) or the gingival oral epithelium (study group 2, comprising another 30 chronic periodontitis patients), adjacent to teeth with poor prognosis. Standard two-step immunohistochemistry and semi-quantitative evaluation of immunohistochemical staining were used to determine syndecan-1 expression. Statistical analyses on the impact of various putative factors were performed., Results: In the junctional/pocket epithelium or the oral epithelium, syndecan-1 expression was weak to moderate in the suprabasal and basal epithelial cells and absent to weak in the internal basal lamina, external basal lamina and gingival connective tissue matrix. Syndecan-1 expression in the junctional/pocket epithelium was statistically significantly stronger than in the oral epithelium in inflammatory cells within the underlying gingival connective tissue (primarily plasma cells and lymphocytes) and in scattered fibroblast-like cells., Conclusions: Syndecan-1 expression in the junctional/pocket epithelium or the oral epithelium can exhibit a significant positive correlation with the severity/degree of histologically evaluated local gingival inflammation, but in general is not significantly correlated with age, smoking, full-mouth and local clinical (probing pocket depth and clinical attachment level) and radiographical parameters (radiographical bone loss) of periodontal status.

Background and Objective: Because human gingival fibroblasts (HGFs) are the predominant cells in periodontal tissues, we hypothesized that HGFs are contributed to receptors for components of bacteria. In this study, we focused on expression and function of nucleotide binding oligomerization domain 2 (NOD2) in HGFs, which is a mammalian cytosolic pathogen recognition molecule., Material and Methods: Expression of NOD2 in HGFs was examined by reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry. Production of interleukin (IL)-6, IL-8, cc chemokine ligand2, cxc chemokine ligand10 (CXCL10) and CXCL11 from HGFs was examined by enzyme-linked immunosorbent assay (ELISA). We used RT-PCR and immunohistochemistry to detect the NOD2 expression in human gingival tissues., Results: We found clear NOD2 expression in HGFs. Upon stimulation with NOD2 agonist, muramyldipeptide (MDP), production of proinflammatory cytokines was enhanced. Moreover, MDP-induced production of proinflammatory cytokines was inhibited in a different manner by mitogen-activated protein kinase inhibitors and phosphatidylinositol 3-kinase inhibitor. Furthermore, MDP enhanced CXCL10 and CXCL11 productions by tumor necrosis factor-alpha (TNF-alpha)- or interferon-gamma (IFN-gamma)-stimulated HGFs, although MDP alone did not induce these chemokines. TNF-alpha and IFN-gamma increased NOD2 expression in HGFs. In addition, we detected NOD2 expression in mononuclear cells and HGFs in periodontally diseased tissues., Conclusion: These findings indicate that MDP which induces production of cytokines and chemokines from HGFs is related to the pathogenesis of periodontal disease.

Background and Objective: Visible, near-infrared (optical) spectroscopy can be used to measure regional tissue hemodynamics and edema and therefore may represent an ideal tool with which to study periodontal inflammation in a noninvasive manner. The study objective was to evaluate the ability of optical spectroscopy to determine simultaneously multiple inflammatory indices (tissue oxygenation, total tissue hemoglobin, deoxyhemoglobin, oxygenated hemoglobin and tissue edema) in periodontal tissues in vivo., Material and Methods: Spectra were obtained, processed and evaluated from healthy, gingivitis and periodontitis sites (n = 133) using a portable optical, near-infrared spectrometer. A modified Beer-Lambert unmixing model that incorporates a nonparametric scattering loss function was used to determine the relative contribution of each inflammatory component to the overall spectrum., Results: Optical spectroscopy was harnessed to generate complex inflammatory profiles of periodontal tissues. Tissue oxygenation at periodontitis sites was significantly decreased (p < 0.05) compared to sites with gingivitis and healthy controls. This was largely the result of an increase in deoxyhemoglobin in the periodontitis sites compared with healthy (p < 0.01) and gingivitis (p = 0.05) sites. Tissue water content per se showed no significant difference between the sites, but a water index associated with tissue electrolyte levels and temperature differed significantly between periodontitis sites and both healthy and gingivitis sites (p < 0.03)., Conclusion: This study established that optical spectroscopy can simultaneously determine multiple inflammatory indices directly in the periodontal tissues in vivo. Visible, near-infrared spectroscopy has the potential to be developed into a simple, reagent-free, user-friendly, chairside, site-specific, diagnostic and prognostic test for periodontitis.

Background and Objective: This study is a systemic review of coronally positioned flap, coronally positioned flap+chemical root surface conditioning, or coronally positioned flap+enamel matrix derivative (EMD) for the treatment of Miller class I and II gingival recession., Material and Methods: All studies available through the Medline database by the end of October 2005 were used. Each study provided mean clinical attachment level, keratinized tissue, probing pocket depth, gingival recession depth and root coverage percentage before and after treatment with coronally positioned flap alone, coronally positioned flap+chemical root surface conditioning, or coronally positioned flap+EMD. Effectiveness was evaluated by comparing the weighted mean average in gingival recession depth, probing pocket depth, clinical attachment level, keratinized tissue and root coverage percentage achieved with the three treatments., Results: Seven studies for the coronally positioned flap+EMD group, four studies for the coronally positioned flap+chemical root surface conditioning group, and seven studies for the coronally positioned flap group were retrieved for this weighted mean analysis. The results of clinical attachment level, gingival recession depth, and root coverage percentage in the coronally positioned flap+EMD group were statistically significantly better than the changes in the coronally positioned flap and coronally positioned flap+chemical root surface conditioning group at 6 and 12 mo (p<0.001). There was no significant difference at the 6-mo comparison among clinical attachment level, keratinized tissue, probing pocket depth, and gingival recession depth, except in the root coverage percentage for coronally positioned flap and coronally positioned flap+chemical root surface conditioning groups., Conclusion: The results suggest that root coverage by the coronally positioned flap and coronally positioned flap+chemical root surface conditioning procedures were unpredictable but became more predictable when the coronally positioned flap procedure was improved by the modification of adding EMD.

Background: Mast cells are a prominent cell type in the gingival infiltrate in periodontitis. In this study we examined the expression by gingival mast cells of matrix metalloproteinases, MMP-1, MMP-2, MMP-8 and the tissue inhibitors of metalloproteinases, TIMP-1 and TIMP-2., Methods: Gingival specimens from 12 human immunodeficiency virus-negative (HIV-) and 15 HIV-positive (HIV+) patients with chronic marginal periodontitis (CMP), and from 10 HIV- and four HIV+ controls with clinically healthy gingiva (HG) were examined after double immunofluorescence staining for mast cell tryptase, combined with antibodies for MMP-1, MMP-2, MMP-8 or their inhibitors TIMP-1 and TIMP-2., Results: In the HIV+CMP, HIV+HG and HIV-CMP groups, all mast cells expressed MMP-1 and MMP-8, whereas a smaller proportion (40-60%) in the HIV-HG controls displayed such staining. The former groups also displayed a significantly higher proportion (39-64%) of mast cells expressing MMP-2 as compared with the HIV-HG group (21-31%). All groups displayed similar proportions of TIMP-1 expressing mast cells (86-100%), whereas significantly increased proportions of TIMP-2+ mast cells were seen in the HIV+CMP, HIV+HG and HIV-CMP groups (18-25%) as compared with the HIV-HG group (8-13%). Mast cells were the cell type that most prominently expressed MMP-1 and MMP-8. MMP-2 expression was also strong in mast cells, but was also similarly expressed in other cell types., Conclusion: The chronically inflamed periodontal lesions in the present study appeared with little evidence of mast cell degranulation. The results show, however, that mast cells in inflamed gingiva have the potential to degrade extracellular matrix if appropriately triggered.

Objective: The aim of the present study was to investigate whether interleukin (IL)-1beta in diseased tissues adjacent to periodontal pockets can reflect the degree of inflammation and destruction of these tissues pathologically., Background: IL-1beta-dependent mechanisms have been strongly implicated in contributing to inflammation and destruction of bone and attachment loss, which are characteristic features of periodontal disease. This biochemical mediator released during pro-inflammatory processes has not been objectively integrated with clinical and histopathologic features of periodontal disease., Methods: Periodontitis-affected inflamed tissue and clinically nonaffected healthy gingivae were harvested from 14 periodontal patients, respectively. The severity of tissue inflammation was illustrated by clinical parameters and cellular histologic changes and quantified by histometric assessments. IL-1beta in these extracted specimens was measured with an enzyme-linked immunosorbent assay (ELISA) technique. Pathogenic roles that IL-1beta plays in gingival inflammation and pathologic tissue changes in tissue sections were analyzed statistically., Results: The overall total tissue IL-1beta, tissue concentration of IL-1beta, and percentage of inflammatory cell infiltration (PICI) determined from diseased gingivae were obviously higher than those of controls from both healthy sites of periodontitis and non-periodontitis subjects. With increasing gingival index (GI), plaque index (PlI), and probing depth (PD), there was a marked elevation in total tissue IL-1beta. Total tissue IL-1beta was significantly correlated with GI, PlI, the PICI, and tissue alterations. Polymorphonuclear leukocytes (PMNs) and monocyte-macrophage cells seemed to predominate in heavily infiltrated areas of diseased gingiva. These cell types were confirmed by immunocytochemical localization with either monoclonal mouse antihuman neutrophil elastase antibody or monoclonal mouse antihuman macrophage (CD68) antibody, respectively. Total tissue IL-1beta and the PICI were also elevated in diseased gingivae near deeper PD, while neither total IL-1beta nor tissue concentration was statistically correlated with PD. Thus, correlation analysis indicates that IL-1beta level in inflamed periodontal tissues correlates highly with clinical parameters (GI and PlI) and PICI (the degree of inflammation)., Conclusions: These observations suggest that IL-1beta plays a significant role in the pathogenic mechanisms of periodontal tissue destruction, and that measurement of tissue IL-1beta would be a valuable aid and useful for diagnostic markers of periodontal diseases.

Objective: This study assessed associations between the number of standardized scaling strokes and the reduction of endotoxin on the root surface., Background: Therapy of periodontally involved teeth attempts removal of accretions by scaling and root planing. The amount of mechanical therapy required to free the root surface from etiologic factors remains unknown., Methods: Twenty-four extracted human caries-free single rooted teeth with at least 5 mm attachment loss were used. A region of interest (ROI) which contained subgingival calculus was defined on the root surface of each tooth. Standardized force instrumentation was applied using a force-measuring curet. Fifty working strokes were applied to every ROI. Forces applied were recorded. The force recordings were converted from Millivolts into Newtons (N). After every unit of 5 strokes, presence of calculus was evaluated and scaling debris was collected. Endotoxin concentration was determined in the debris samples., Results: The endotoxin values for strokes 1-5 were statistically significantly greater than the values from all other stroke intervals. Complete calculus removal occurred after a mean of 9.3 strokes. The endotoxin concentration reached a minimal level with concentrations of 0.03-0.306 EU/ml after calculus removal was complete., Conclusion: These findings suggest that completion of calculus removal coincides with endotoxin levels associated with clinically healthy teeth.

Proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) was found in inflamed periodontal tissues and many studies pointed to its significant role in development of periodontal disease. In this study, the influence of subcutaneously administered recombinant human TNF-alpha (rhTNF-alpha) on inflammatory reaction and periodontal breakdown in rats was analyzed during experimental periodontitis, induced by placing silk ligatures around the maxillary right second molar tooth. The rats were divided into two groups with five animals in each; the first group was infused subcutaneously with rhTNF-alpha via osmotic pumps for 2 weeks and the second group was infused with phosphate-buffered saline (PBS) in the same manner. Inflammatory reaction and periodontal breakdown was evaluated morphometrically on hematoxylin and eosin stained sections. Serum ionized calcium and inorganic phosphates were monitored colorimetrically. Serum calcium and phosphate levels were similar in rats receiving rhTNF-alpha and PBS. Ligation resulted in accelerated periodontal breakdown, while subcutaneous rhTNF-alpha administration by itself had no significant effect. Combined effect of subcutaneous rhTNF-alpha administration and ligation resulted in a significantly greater inflammatory reaction and periodontal breakdown then either treatment alone. We concluded that the subcutaneous administration of rhTNF-alpha accelerates the progression of experimental periodontitis in rats.

The hippocampus, which is a brain structure involved in learning and memory processes, plays a key role in the feedback regulation of the hypothalamic-pituitary-adrenal (HPA) axis and autonomic sympathetic nervous system, and the subsequent secretion of immuno-modulatory hormones in response to pathogenic microorganisms. Dysregulation of these brain-neuroendocrine-immune regulatory networks, which act in concert to maintain homeostasis, is found to be of critical importance to the host defence against pathogens, as well as susceptibility to diseases, including periodontal disease. The present study was designed to determine the effects of hippocampal lesioning on the progression of periodontitis. Experimental ligature-induced periodontitis was induced in 16 Wistar rats, which were bilaterally lesioned in their hippocampal region with an aspiration technique that is well documented to impair learning and memory, as well as in 15 sham-operated control rats. The disease progression was evaluated radiographically and histometrically. The results revealed that the hippocampal lesioned rats developed significantly more destruction of the periodontium than did the sham-operated controls. This finding supports recent studies that indicate that inappropriate brain-neuroendocrine regulation of inflammatory responses to infectious agents may play an important role in disease susceptibility and progression.

Leukocyte migration is essential for immune surveillance of tissues by focusing immune cells to sites of antigenic challenge. The control of leukocyte migration depends on the combined actions of adhesion molecules and a vast array of chemokines and their receptors. The purpose of the present study was to investigate the involvement of Interleukin-8 (IL-8), RANTES, the associated infiltrating cells and expression of CCR5 chemokine receptors in periodontitis; furthermore, the effect of periodontal therapy on these parameters was evaluated. Patients included in the study had moderate to advanced periodontal disease with at least 5-6 teeth with probing depth > 6 mm, attachment loss > or =3 mm and extensive radiographic bone loss. The inflammatory infiltrate was analyzed by immunohistochemistry in gingival biopsies obtained from subjects at the beginning of the study and 2 months after periodontal treatment. Gingival crevicular fluid (GCF) was collected for 30 seconds using periopaper strips, and chemokines were quantified by ELISA. The cellular components of the inflammatory infiltrate included B (CD19) and T (CD3, CD4+ and CD8+) lymphocytes and monocytes/macrophages (CD11c). CCR5 chemokine receptor expressing cells were exclusively found in periodontitis gingiva. IL-8 and RANTES were detected in the periodontitis group, obtaining a total amount of 212.5 pg and 42.0 pg, respectively. However, IL-8 was also detectable in the GCF of the healthy group (total amount of 44.8 pg). Periodontal therapy reduced the cell number in the infiltrate and the levels of IL-8 and RANTES, suggesting a relationship between these chemokines and periodontal status. We propose that the presence of these chemokines and the expression of chemokine receptors may represent a marker of lymphocyte subsets with the ability to migrate to inflammatory sites.

Cigarette smoking is a potential risk factor which has recently been associated with periodontal disease progression. The objective of this study was to compare the microbial profile of smokers and non-smokers in a group of patients with early onset periodontitis. The study population consisted of 60 healthy individuals, 40 males and 20 females aged 22 to 35 yr, exhibiting early onset periodontitis. Thirty patients were smokers (30.9 cigarettes/d) and 30 non-smokers. Smokers had a higher proportion of deep pockets (PD >5 mm), especially in the maxilla anterior and premolar regions (p < 0.001) and presented a significantly greater mean probing depth and attachment loss (p <0.05) in diseased sites and a significantly greater alveolar bone loss (p <0.01) compared to non-smokers. Two pooled bacterial samples were obtained from each patient. Samples were collected from the deepest periodontal pockets of each quadrant. The samples were cultured anaerobically and in 10% CO2 plus air for bacterial isolation using selective and non-selective media. Isolates were characterized to species level by conventional biochemical tests and various identification kits. Smokers harboured a greater number of bacteria in total. Analysis of bacterial counts using the ANOVA (Mann-Whitney U-test) showed that Staphylococcus aureus, Peptostreptococcus micros, Campylobacter concisus, Escherichia coli, Bacteroides forsythus, C. gracilis, C. rectus, Porphyromonas gingivalis, Selenomonas sputigena, Candida albicans and Aspergillus fumigatus were found in significantly higher numbers and more frequently in smokers while Streptococcus intermedius, A. naeslundii, A. israelii and Eubacterium lentum were detected more frequently and in significantly higher proportions in non-smokers. The isolation of bacteria belonging to the exogenous flora such as E. coli, C. albicans, A. fumigatus and S. aureus in smokers' microbiota underscores the importance of the host that is adversely affected by cigarette smoking.

The classification of periodontitis in various disease categories, including juvenile periodontitis, rapidly progressive adult periodontitis and slowly progressive adult periodontitis is based mainly on differences in disease progression and age group susceptibility. Because dissolution of collagen fibers is an integral part of periodontal attachment loss, we investigated whether the clinical differences among these periodontitis/control groups are reflected in the collagen-degrading activity of gingival fibroblasts isolated from affected tissues. All fibroblast strains isolated from the 4 groups (n = 48) displayed cell-associated collagenolytic activity when seeded in contact with a reconstituted film of type I collagen fibrils. Cells from the control group (n = 14) dissolved the collagen fibril film twice as fast as those from each of the 3 disease groups (juvenile periodontitis (n = 13), rapidly progressive adult periodontitis (n = 7), and slowly progressive adult periodontitis (n = 14)). Both interleukin-1 beta and phorbolester accelerated the rate of dissolution 2-4-fold, but even after cytokine or phorbolester stimulation control cells were still considerably more effective in dissolving the collagen fibrils than cells from the disease groups. The observation made in this study, that dissolution of collagen fibrils by gingival fibroblasts from periodontally diseased individuals is significantly slower than by cells from healthy control subjects, challenges disease paradigms based on a direct relationship between collagenolytic potential and disease activity.

Change in clinical attachment level (CAL) and radiographic change in crestal bone height are often used to assess periodontal breakdown and disease progression. These two variables are also used to monitor the effect of treatment. The purpose of the present longitudinal study was to evaluate the correlation between changes in CAL and alveolar bone loss. Following initial screening, 79 subjects with established periodontitis were monitored quarterly for 1 yr, using a pressure-sensitive automated probe. CAL and relative attachment level (RAL) were recorded at 6 sites for each tooth. Radiographs were obtained at baseline and 1 yr. Crestal bone changes were determined using an image enhancement technique. Mean change in attachment level was 0.16 mm. Similarly, mean proximal bone loss measured radiographically was 0.16 mm. In 6.9% of all the sites, and 13.7% of all pooled interproximal sites, AL loss was in excess of the threshold defined as 2 s.d. of repeated measurements (mean 1.54 mm). Similar percentages of sites (12.9%) had radiographic evidence of proximal bone loss exceeding the threshold (0.55-1.08 mm). A site-based analysis of active sites revealed an overall poor correlation between the 2 variables (kappa value = 0.03) which was the result of a very poor sensitivity (0.16) despite a relatively good specificity (0.81). A patient-based comparison of clinical and radiographical changes revealed an overall kappa value of 0.08, with sensitivity and specificity of 0.51 and 0.56, respectively. However, baseline CAL and crestal bone height showed good correlation (r = 0.73; p = 0.0001). It is suggested that changes in CAL and radiographic bone level progress somewhat independently. Over a short-term period of time they might not follow the same course; however, in the long term, these differences seem to level off. For longitudinal monitoring of disease progression and response to therapy both methods may be needed; while for cross-sectional evaluation and long-term prospective studies, either variable may be used alone.

The purpose of this meta-analysis was to provide a quantitative overview of clinical trials assessing the use of systemic metronidazole (S-MET) as an adjunct to scaling and root planning (S&RP) in the treatment of adult periodontitis. Eight clinical trials were chosen based upon a priori selection criteria, and two outcomes, "reduction in probing pocket depth" (PD) and "gain in clinical attachment level" (CAL), were analyzed. Results for each outcome were stratified by initial PD 1-3 mm, 4-6 mm, or > or = 7 mm and length of follow-up 4-6 wk, 9-13 wk, or 14-26 wk. S-MET in conjunction with S&RP was superior to S&RP alone in reducing PD where initial PD was 4-6 mm and follow-up was 9-13 wk (0.43 mm; 99% CI 0.12, 0.73). No significant advantage was observed for S-MET for reducing PD where initial PD was less than 4 mm or follow-up was longer than 13 wk. S-MET in conjunction with S&RP was superior to S&RP alone in reducing CAL where initial PD was 4-6 mm and follow-up was 4-6 wk (0.29; 99% CI 0.01, 0.58) and where follow-up was 9-13 wk (weighted mean difference 0.32; 99% CI 0.03, 0.61). Significant heterogeneity of effect was not seen for PD or Cal at any level of initial PD or length of follow-up. No significant dose-response relationship was observed. This meta-analysis was limited due to diversity of data presentation and the small number of trials in each stratum. These results suggest that S-MET in conjunction with S&RP may offer a benefit over S&RP alone in the treatment of adult periodontitis patients in managing pockets of 4 mm or greater, but the additional benefit was not evident if initial PD was less than 4 mm or follow-up was beyond 13 wk.

Interleukin-1 (IL-1) molecules, IL-1 alpha and IL-1 beta are cytokines involved in the acute-phase response against infection and in the pathogenesis of periodontal destruction. Administration of exogenous IL-1 receptor antagonist (IL-1ra) is effective in reducing the inflammatory reactions mediated by IL-1. However, the relationship between these three naturally occurring IL-1 molecules and periodontal diseases has been poorly characterized. We investigated the correlation of gingival crevicular IL-1 molecules and the clinical status of patients with different severities of periodontitis. IL-1 alpha, IL-1 beta, IL-1ra and the total IL-1/IL-1ra ratio (IL-1 activity index; IL-1AI) were measured in 75 gingival crevicular fluid (GCF) samples from non-inflamed gingiva sites in 2 healthy subjects and diseased sites in 7 patients with several types of periodontitis. IL-1 alpha, IL-1 beta and IL-1ra were measured by specific non-cross-reactive enzyme linked immunosorbent assay. The probing depth, gingival index and alveolar bone loss of each site was recorded at the time of GCF sampling. The total amount of IL-1 alpha, IL-1 beta and the IL-1AI, but not total IL-1ra, were found to be correlated with alveolar bone loss score. Three IL-1 molecules were also measured in the gingival tissue of patients with periodontitis. A similar progressive decrease of the IL-1AI was detected in gingival tissue with periodontitis. These results suggest that the amounts of both crevicular IL-1 and IL-1AI are closely associated with periodontal disease severity.

Most of our knowledge regarding the natural history of periodontitis in adults has come from clinical studies of dental patients. However, it is known that dental patients usually are not representative of what actually happens in the population. This paper presents population-based attachment loss trends in survivor teeth to address the following issues; 1) whether attachment loss during 1 period in time is associated with higher risk for attachment loss at a subsequent period in the same subject; 2) whether sites in survivor teeth with deeper periodontal pockets at baseline are more likely to experience future attachment loss; and 3) whether the effect of regular use of dentists' services on attachment loss are demonstrated in a community-dwelling population. In 1988, the University of North Carolina School of Dentistry initiated the Piedmont 65+ Dental Study, which was designed to elicit 800 dentate respondents in the 5-county area who were examined again at 18, 36 and 60 months. Our findings indicated that, for the 3 time periods investigated, attachment loss during the first period was not related to the incidence of attachment loss at a subsequent period for most people. However, for people who experience multiple episodes, the second episode was likely to immediately follow the first episode. This pattern did not occur at the site level where no site experienced more than 2 successive episodes, and a previous episode did not put a site at higher risk for a subsequent episode. Our data also indicated that both baseline pocket depth and irregular dental visits were positively associated with the proportion of sites that demonstrated break-down over the next 5 yr.

The aim of the present study was to investigate whether incipient periodontal disease breakdown could be associated with changes in gingival crevicular fluid (GCF) acute-phase protein levels. In addition, the potential of clinical indices to act as predictors of significant attachment level (AL) change was investigated. AL measurements were taken at baseline and 3 months using the Florida Probe stent handpiece from a total of 384 sites in 38 patients. The average standard deviation of duplicate AL measurements was 0.423. When the tolerance method was used to detect significant AL change, 3.9% of the sites lost attachment. When a less stringent criterion of AL change of > or = 1 mm was used 9.9% of the sites lost attachment during the 3-month period. With the exception of probing depth, baseline clinical parameters failed to predict AL change. Fourteen active periodontitis sites that demonstrated significant attachment loss were paired to stable periodontitis sites within the same patient. The levels of four acute-phase proteins, namely alpha 2-macroglobulin (alpha 2-M), alpha 1-antitrypsin (alpha 1-AT), transferrin (TF) and lactoferrin (LF), and also albumin (Alb) were assessed in the same gingival crevicular fluid sample using sandwich ELISAs. Results were expressed either as ng/30 s and ng/microgram Alb. Acute-phase protein levels in GCF failed to differentiate between active and stable periodontitis sites at baseline. In conclusion, the degree of gingival inflammation of the tissues adjacent to the crevice/pocket seems to influence the levels of protease inhibitors and iron-binding proteins in GCF to a greater extent than probing attachment loss.

The stepwise approach to the determination of periodontal attachment loss involves fitting linear, logarithmic, and exponential models to individual site data and concluding that the form of loss is consistent with the model that has the greatest r-value, provided that the model predicts loss in excess of a site-specific threshold. Logarithmic and exponential fits are considered to define early and late bursts, respectively, while linear fit describes loss at a constant rate. In a recently published study, the stepwise approach was applied to 6,935 sites in patients with established periodontitis and, of 581 loss detections, 195 (33.6%) were linear, 224 (38.6%) logarithmic, and 162 (27.9%) exponential. However, curvilinear patterns may occur by chance and regression algorithms that can fit such curvature may have an advantage unrelated to the true mechanism(s) [correction of mchanism(s)] of periodontal destruction. To investigate the implications of this possibility, proportions of linear, logarithmic, and exponential fit were estimated by simulation under four different conditions. These conditions incorporated random or random plus linear change, but no nonlinear effects. The relative proportions of model fits described in the published study were approximated in all of these conditions. It would appear that the observed proportions are ubiquitous to the modelling approach itself, and do not constitute evidence of a causal non-linear biological mechanism. The stepwise approach may be useful for detecting change but relevance to causal processes seems problematic.

Serial attachment level measurements were simulated based on 2 hypothetical models of true change: 1) a burst model, where attachment changes rapidly over the duration of one measurement interval, but is unchanging before and after, and 2) a linear model, where attachment changes at a constant rate over time. Normally distributed measurement error was added to the modeled attachment level change to produce the series of measurement simulations. It was then determined for each series whether a burst model or a linear model best fit the simulated measurement series for a range of overall attachment level changes. For series generated by a burst model, the burst model fit better than a linear model a significant proportion of the time at all attachment level changes. However, for series generated by a linear model, the burst model provided the best fit for attachment level changes that were less than 4 times the standard deviation of the measurement error. Estimates of change based on a linear model slightly overestimated change when the true underlying model was a burst model. Estimates of change based on a burst model slightly underestimated change when the true model was a burst model, but substantially underestimated change when the underlying model was a linear model. Model fit when assessed by the least squares criterion may not be a reliable guide to model validity.

The purpose of this investigation was to study the microflora of severe, moderate and minimal periodontal lesions, in young adults with rapidly progressive periodontitis (RPP). Subgingival plaque samples were taken from 142 periodontal lesions in 10 young adults aging 25 to 35 years. The examination of the subgingival microflora indicated that certain species, including Porphyromonas gingivalis, Bacteroides forsythus, Fusobacterium nucleatum, Actinobacillus actinomycetemcomitans, and Campylobacter species were found to be predominant in severe periodontal lesions. B. forsythus, P. gingivalis, Prevotella intermedia, F. nucleatum, Capnocytophaga ochracea, were predominant in medium lesions while Streptococcus species and Actinomyces species, C. ochracea, Haemophilus segnis and Veillonella parvula, were found in higher levels in minimal periodontal lesions.