Chronic treatment with the glucocorticoid receptor antagonist RU486 inhibits diabetes-induced enhancement of experimental periodontitis.

BACKGROUND AND OBJECTIVE: Chronic hypothalamic-pituitary-adrenal (HPA) axis hyperactivity and excessive glucocorticoid hormone release have been associated with diabetes, altered immune responses and increased susceptibility to periodontitis. In the present study we tested the impact of streptozotocin (STZ)-induced diabetes on ligature-induced periodontitis and the effect of subsequent treatment with the glucocorticoid receptor (GR) antagonist, RU486. MATERIAL AND METHODS: A single dose of STZ [45 mg/kg, intraperitoneally (i.p.)] or vehicle was given 10 d before induction of ligature-induced periodontitis and implantation subcutaneously of a drug pellet containing the GR antagonist, RU486, or a placebo pellet. Periodontitis was assessed when the ligatures had been in place for 21 d. Two hours before decapitation all rats received gram-negative bacterial lipopolysaccharide (LPS) (150 µg/kg, i.p.) to induce a robust immune and stress response. RESULTS: Compared with control rats, STZ-treated rats developed significantly more periodontal bone loss, and RU486 treatment of STZ -treated rats significantly inhibited this effect. STZ-treated rats also showed significantly higher levels of the HPA axis-derived hormone, corticosterone, as well as of the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-α), but lower levels of the anti-inflammatory cytokines interleukin-10 (IL-10) and transforming growth factor-1beta (TGF-1ß) after LPS stimulation. GR blockade had no statistically significant effects on these measurements in diabetic rats, but tended to enhance the levels of TNF-α and TGF-1ß, and reduce the levels of IL-10 and blood glucose. CONCLUSION: In diabetic subjects, excessive GR activation as a result of chronic high levels of glucocorticoid hormones may alter immune-system responses in a manner that may increase the susceptibility to periodontitis.

Oral treatment with complement factor C5a receptor (CD88) antagonists inhibits experimental periodontitis in rats.

BACKGROUND AND OBJECTIVE: The complement activation product 5a (C5a) is a potent mediator of the innate immune response to infection, and may thus also importantly determine the development of periodontitis. The present study was designed to explore the effect of several novel, potent and orally active C5a receptor (CD88) antagonists (C5aRAs) on the development of ligature-induced periodontitis in an animal model. MATERIAL AND METHODS: Three different cyclic peptide C5aRAs, termed PMX205, PMX218 and PMX273, were investigated. Four groups of Wistar rats (n = 10 in each group) were used. Starting 3 d before induction of experimental periodontitis, rats either received one of the C5aRas (1-2 mg/kg) in the drinking water or received drinking water only. Periodontitis was assessed when the ligatures had been in place for 14 d. RESULTS: Compared with control rats, PMX205- and PMX218-treated rats had significantly reduced periodontal bone loss. CONCLUSION: The findings suggest that complement activation, and particularly C5a generation, may play a significant role in the development and progression of periodontitis. Blockade of the major C5a receptor, CD88, with specific inhibitors such as PMX205, may offer novel treatment options for periodontitis.

Nicotinic acetylcholine receptor activation mediates nicotine-induced enhancement of experimental periodontitis.

BACKGROUND AND OBJECTIVE: Smokers have an increased risk of developing periodontitis as well as showing more rapid progression and resistance to treatment of the disease, but the biological mechanisms are poorly understood. This study was designed to investigate putative biological mechanisms by which nicotine may enhance the susceptibility and thus the course of periodontitis in an animal model. MATERIAL AND METHODS: Ligature-induced periodontitis was applied in periodontitis-susceptible Fischer 344 rats. The animals were either given daily intraperitoneal injections of the nicotinic acetylcholine receptor antagonist mecamylamine (1 mg/kg) 45 min before subcutaneous injections in the neck skin of nicotine (0.8 mg/kg), or treated with the same amount of saline intraperitoneally and nicotine subcutaneously, or treated with mecamylamine and saline. Control animals received intraperitoneal and subcutaneous injections of saline only. Periodontal bone loss was assessed when the ligatures had been in place for 3 wk. Two hours before decapitation, all rats received lipopolysaccharide (LPS; 100 microg/kg, intraperitoneally) to induce a robust immune and stress response. RESULTS: Compared with saline/saline-treated control animals, saline/nicotine-treated rats developed significantly more periodontal bone loss, and LPS provoked a significantly smaller increase in circulating levels of the cytokines tumour necrosis factor-alpha, transforming growth factor-1beta and interleukin-10. Mecamylamine pretreatment of nicotine-treated rats abrogated the increased periodontal bone loss and the LPS-induced decrease in tumour necrosis factor-alpha, but had no significant effects on the levels of transforming growth factor-1beta and interleukin-10, or the stress hormone corticosterone. CONCLUSION: The results indicate that nicotine enhances the susceptibility to periodontitis via nicotinic acetylcholine receptors, which may act by suppressing protective immune responses through the cholinergic anti-inflammatory pathway.

Nicotinic acetylcholine receptor activation mediates nicotine-induced enhancement of experimental periodontitis.

BACKGROUND AND OBJECTIVE: Smokers have an increased risk of developing periodontitis as well as showing more rapid progression and resistance to treatment of the disease, but the biological mechanisms are poorly understood. Our objective was to investigate putative biological mechanisms by which nicotine may enhance the susceptibility and thus the course of periodontitis in an animal model. MATERIAL AND METHODS: Ligature-induced periodontitis was applied in periodontitis-susceptible Fischer 344 rats. The animals were given daily intraperiotonal (i.p.) injections of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine (1 mg/kg) 45 min before subcutaneous (s.c.) injections in the neck skin with nicotine (0.8 mg/kg), or treated with the same amount of saline i.p. and nicotine s.c., or with mecamylamine and saline. Control rats received i.p. and s.c. injections of saline only. Periodontal bone loss was assessed when the ligatures had been in place for 3 weeks. Two hours before decapitation, all rats received lipopolysaccharide (LPS; 100 microg/kg, i.p.) to induce a robust immune and stress response. RESULTS: Compared with saline/saline-treated control rats, saline/nicotine-treated rats developed significantly more periodontal bone loss, and LPS provoked a significantly smaller increase in circulating levels of the cytokines tumour necrosis factor alpha (TNF-alpha), transforming growth factor 1beta (TGF-1beta) and interleukin-10 (IL-10). Mecamylamine pretreatment of nicotine-treated rats abrogated the increased periodontal bone loss and the LPS-induced TNF-alpha decrease, but had no significant effects on the levels of TGF-1beta and IL-10, or the stress hormone corticosterone. CONCLUSION: The results indicate that nicotine enhances susceptibility to periodontitis via nAChRs, which may act via suppressing protective immune responses through the cholinergic anti-inflammatory pathway.

Relationship between knowledge and attitudes regarding HIV/AIDS among dental school employees and students.

OBJECTIVES: Employees and students at the Faculty of Dentistry, University of Oslo responded to a comprehensive questionnaire regarding knowledge and attitudes towards human immunodeficiency virus (HIV). The intention of the present study was to describe possible relationships between the two. METHOD: The questionnaire consisted of 39 closed questions. The response rate was 75% (436/584). The answers were used to construct additive indices for knowledge and attitudes. RESULTS: The knowledge index reflected the number of correct answers concerning risk groups and transmission. A factor analysis revealed three dimensions of attitudes ('legal', 'personal risk', and 'personal consequences'), which were analysed separately against knowledge. Correlation analyses (Spearman r) of all respondents together (n = 436) revealed a weak, but statistically significant, positive correlation between knowledge and the 'legal' and 'personal risk' dimension of attitudes (r = 0.16, P < 0.01; r = 0.21, P < 0.001). The 'personal consequence' dimension was not significantly correlated with knowledge (r = 0.06, P > 0.05). The strongest correlation was found between knowledge and the 'legal' dimension (r = 0.43, P < 0.001), and knowledge and the 'personal risk' dimension (r = 0.41, P < 0.002) amongst fourth year students. No particular group of employees or students displayed a significant correlation between knowledge and the 'personal consequence' dimension of attitudes. CONCLUSIONS: Three dimensions on attitudes concerning patients with HIV/acquired immune deficiency syndrome were identified amongst the respondents. A weak correlation between knowledge and two of the attitudes might indicate that knowledge plays a role in this respect.

Effects of hippocampal lesioning on experimental periodontitis in Wistar 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.

Treatment of dentin hypersensitivity by Nd:YAG laser.

BACKGROUND, AIMS: Promising results using Nd:YAG laser against dentin hypersensitivity have been reported. The aim of this double-blind, controlled, split-mouth designed clinical trial was to assess the effect of a single Nd:YAG laser application on alleviating hypersensitivity. METHODS/RESULTS: Seventeen subjects participated in the study. Each of them had two teeth treated; one with the laser activated and one with nonactivated (placebo), for 2 min The assessment of pain was performed by a VAS, after an air blast at baseline immediately after treatment, at 1 week, 4 weeks and 16 weeks. Mean values of VAS for test and control teeth were compared by paired t-test (alpha = 0.05). The results showed mean baseline VAS values of 6.59 (+/- 1.65) and 6.14(+/- 1.95) for test and control teeth, respectively. Immediately after treatment, these values decreased to 4.09(+/- 2.28) and 3.89(+/- 2.11), respectively. After 1 week, 4 weeks and 16 weeks the mean values for test and control teeth were 3.85 +/- 2.36, 4.03 +/- 1.95, 3.60 +/- 2.66, and 4.44 +/- 2.56, 3.41 +/- 2.30, 3.42 +/- 2.30, respectively. There were no statistically significant differences between test and control at any time. However, both groups improved significantly (P < 0.05) from baseline to immediately after application, and at 1 week, 4 weeks and 16 weeks, respectively. The changes that occurred between immediately after application and 1 week, 4 weeks and 16 weeks, respectively, were not statistically significant. CONCLUSION: It is concluded that the effect of treatment of hypersensitive teeth with Nd:YAG laser is not different from placebo. The observed effects seem to last for at least 16 weeks.

Postnatal glutamate-induced central nervous system lesions alter periodontal disease susceptibility in adult Wistar rats.

BACKGROUND: Inability to mount a suitable brain-neuroendocrine response to bacterial or other antigenic challenges has been found to play an important rôle in infectious and inflammatory disease susceptibility and progression, including periodontal disease. OBJECTIVE: The present study was designed to determine the effects of glutamate administration to new-born Wistar rats on the development and progression of naturally occurring and ligature-induced periodontal disease in the rats as adults. Postnatal glutamate administration is known to permanently damage neurones in the hypothalamic arcuate nucleus. METHOD: New-born rats were treated 1x daily subcutaneously with 2 mg/g of monosodium-L-glutamate (MSG) for 5 days from day 3 to 6. Control animals were injected with similar amounts of saline. Experimental ligature-induced periodontal disease was induced in the rats at the age of 12 weeks at maxillary right 2nd molar teeth. The contralateral maxillary left 2nd molars served as control teeth, and for assessment of naturally occurring periodontal disease. Disease progression was evaluated histometrically. RESULTS: The results revealed that the glutamate-lesioned rats developed significantly more periodontal tissue destruction compared to sham-lesioned control rats in both the ligated and non-ligated teeth. CONCLUSIONS: This study supports our recent findings indicating that inappropriate brain-neuroendocrine-immune regulation may play a rôle in periodontal disease susceptibility and progression.

Hypothalamic-pituitary-adrenal axis activation by experimental periodontal disease in rats.

Organisms respond to inflammatory conditions by mounting a co-ordinated complex series of adaptive responses involving the immune, nervous and endocrine systems that are aimed at restoring the homeostatic balance. We have recently shown in a rat model that inappropriate hypothalamic-pituitary-adrenal (HPA) axis regulation and a subsequent inability to mount a suitable glucocorticoid response to gingival inflammation may influence susceptibility to periodontal disease. This study was designed to investigate whether ligature- and bacterial lipopolysaccharide (LPS)-induced inflammation in the gingival connective tissues may activate this physiological axis, and to further explore the significance of HPA regulation in periodontal disease. Experimental periodontal disease was induced in major histocompatibility complex (MHC)-identical but HPA low (LEW) and high (F344) responding rat strains. We tested (1) whether ongoing periodontal disease activates the HPA axis as measured by corticosterone levels, and (2) whether genetic differences in HPA regulation modulate periodontal disease progression. In the F344 strain. the periodontal tissue destruction was more severe. This observation was associated with a significant increase of corticosterone levels in F344 rats only. Addition of LPS at the gingival inflammatory site led to a further increase of corticosterone levels and disease severity in F344 rats. These findings illustrate a positive feedback loop between the HPA axis and periodontal disease: the disease activates the HPA axis, and a genetically determined high HPA responsivity further increases disease susceptibility.

Yeasts in periodontal pockets.

OBJECTIVES: The presence of yeasts in periodontal pockets has been described in a few studies. The association between yeasts and putative periodontal pathogens is not well described. This study aims at assessing the prevalence of yeasts in periodontal pockets and possible associations with the clinical conditions of the sampled sites and other micro-organisms present. MATERIAL AND METHODS: 2 subject groups form the basis for this study. The 1st comprises results from microbiological samples from periodontal pockets of 128 subjects. The 2nd originates from 126 periodontal patients with untreated pockets. Microbiological identification was performed after cultivation on blood and Sabouraud agar plates, and "checkerboard" DNA-DNA hybridisation. RESULTS: The prevalence of subjects with yeasts in the pockets was 15.6% and 17.5% in the 2 groups respectively and was inconsistent according to gender. No correlation was found between age and the presence of yeasts. Eubacterium saburreum was weakly correlated with presence of yeasts (r=0.194 p=0.03). Yeasts were rarely found in both samples from the same individual. CONCLUSIONS: Our results indicate that yeasts can be expected to be present in periodontal pockets in one out of 6 periodontal patients independent of gender and age. Eubacterium saburreum seems to occur frequently together with yeasts.

Comparison of oral hygiene efficacy of one manual and two electric toothbrushes.

The purpose of the study was to compare the efficacy of two electric toothbrushes (Philips HP555 and the Philips Jordan 2-action Plaque Remover HP510). A manual toothbrush Jordan V-shaped, medium) served as control. Fifty subjects, aged 18-60 years, participated in a randomized, single-blind, 3 x 3 weeks crossover study. Plaque was assessed according to the Turesky modification of the Quigley-Hein index (P.I.), while the Løe-Silness index was used for assessing gingivitis. Adverse effects were assessed according to the ADA specifications. Compliance and preference were assessed through questionnaires and interviews, respectively. All periods mean P.I. (all surfaces) were 2.79, 3.01, and 2.86 for the manual, the HP555, and the HP510 electric brushes and the corresponding gingivitis values were 1.19, 1.22, and 1.21. For both indices, only the difference between the manual and the HP555 yielded significance (P = 0.04 and P = 0.02). Most subjects (28/50) preferred the HP5 10 brush, as it felt more practical to use and was perceived to have better cleaning ability. In conclusion. no clinically relevant differences in plaque reducing and gingivitis controlling ability were observed.

Glucocorticoid receptor antagonist RU 486 treatment reduces periodontitis in Fischer 344 rats.

Inappropriate hypothalamic pituitary adrenal (HPA) axis regulation of immune responses to bacterial challenges has been found to play an important role in infections and inflammatory disease susceptibility and progression. In the present study we investigated the tissue effects of experimental periodontitis in Fischer 344 rats, which were subcutaneously (s.c.) injected with 20 mg/kg of the glucocorticoid receptor antagonist and active antiglucocorticoid agent RU 486 every second day over a period of 14 d. Periodontitis was induced by placing a bacterial plaque retentive silk ligature in the gingival sulcus around the neck of maxillary right 2nd molar teeth 1 d after the first injection in 10 RU 486-treated and 10 vehicle (1,2-propanediol)-treated control animals. The contralateral maxillary left 2nd molars served as internal control teeth for naturally occurring periodontitis. Disease progression was evaluated radiographically and histometrically. The average level of corticosterone in blood at sacrifice was significantly lower in the RU 486-treated animals as compared to controls. The experimental animals also developed significantly less periodontal breakdown at both experimental and control teeth compared to the vehicle-treated control animals. The results support our recent findings showing that HPA hyper-reactivity, either genetically determined or experimentally induced, stimulates periodontal disease susceptibility. These findings suggest that central nervous regulation of inflammatory responses to dental plaque microorganisms in the gums may modulate periodontal disease susceptibility and progression.

Fc(alpha) receptor I (CD89) on neutrophils in periodontal lesions.

AIMS: In this study, we have examined the occurrence of FcalphaRI-bearing cells in gingival tissue, gingival fluid and blood, in search for possible roles of IgA and FcalphaRI in periodontal lesions. METHODS: Gingival biopsies from inflamed and healthy sites were obtained from patients with chronic marginal periodontitis. Sections of inflamed gingiva were examined by immunofluorescence techniques and compared to sections from healthy sites. Smears were made from blood and gingival crevicular fluid and similarly studied. RESULTS: Dense infiltrates of neutrophils with strong expression of FcalphaRI (and FcgammaRIII) were found in connective tissue and epithelium of the apical part of periodontal pockets from diseased sites. In contrast, only few such cells were found in healthy gingiva from the same patients. Neutrophils in gingival fluid, tissue and blood expressed FcalphaRI with similar intensity, whereas the expression of FcgammaRIII was significantly decreased in gingival crevicular fluid. Considerable numbers of bacteria from gingival plaque were found to be covered by IgA. CONCLUSION: It is suggested that FcalphaRI on neutrophils may play an important rôle in elimination of IgA-opsonized bacteria, both in periodontal tissue and the adjacent pockets.

Effects of hypothalamic-pituitary-adrenal axis reactivity on periodontal tissue destruction in rats.

The aim of this study was to test the hypothesis of an association between hypothalamic-pituitary-adrenal (HPA) axis reactivity and progression of periodontal disease. Histocompatible Lewis and Fischer 344 rats respond to stressful stimuli with low and high HPA axis reactivity, respectively. Experimental periodontitis was induced by tying a silk ligature around the neck of maxillary 2nd right molar teeth in 10 Lewis and 10 Fischer 344 rats with contralateral non-manipulated teeth as controls. Twenty non-manipulated animals were included. Also, experimental periodontitis was induced in 10 adrenalectomized Wistar rats and in 10 sham-operated rats. Furthermore, corticosterone pellets were subcutaneously implanted in 9 Lewis rats, while placebo pellets were implanted in 8 animals. Disease progression was evaluated histometrically and radiographically. The low-responding Lewis rats developed significantly less periodontal breakdown than did the high-responding Fischer 344 rats. Administration of corticosterone increased the disease development. while adrenalectomy reduced the disease severity. Our findings demonstrate the importance of genetic factors in the development of periodontal disease, and suggest that HPA axis hyper-activation is one mechanism by which periodontal disease susceptibility may be increased.

Topical distribution of Fc gammaRI, Fc gammaRII and Fc gammaRIII in inflamed human gingiva.

The topical distribution of Fc gamma receptor types I, II and III (Fc gammaRI-III) was analyzed by means of immunohistochemistry in human gingival tissue obtained from 12 patients with chronic periodontitis. CD68+ macrophages expressing all three classes of Fc gammaR were found throughout the whole gingival connective tissue (CT), whereas dense infiltrates of polymorphonuclear granulocytes (identified by staining for neutrophil elastase) with strong staining for Fc gammaRIII and Fc gammaRII were found subjacent to the apical part of the pocket epithelium (PE) and in the PE itself. CD19+ B lymphocytes with variable staining intensity for Fc gammaRII were observed in clusters subjacent to the PE and extending into the central part of the CT. Only a few scattered CD3+ T lymphocytes stained for Fc gammaRIII. Some spindle-shaped cells (CD68-, therefore non-macrophages) and apparently non-cellular fibrous tissue elements stained for Fc gammaRI and Fc gammaRII. In the epithelium, Fc gammaRII+ dendritic cells were frequently observed in the entire oral gingival epithelium and in the coronal part of the PE. Occasionally, some keratinocytes which stained for Fc gammaRII and Fc gammaRIII were found. The observations indicate that Fc gammaR of the various classes are amply expressed on numerous cell types in inflamed gingival tissue. The specific distribution pattern detected suggests that Fc gammaRs may play a role in the mediation of chronic inflammation in the periodontal lesion.

Clinical and microbiological effects of adjunctive antibiotics in treatment of localized juvenile periodontitis. A controlled clinical trial.

The aim of this study was to assess the clinical and microbiologic effects of the combination of amoxicillin and metronidazole therapy as an adjunct to mechanical treatment in the management of localized juvenile periodontitis. Twenty-five localized juvenile periodontitis (LJP) patients from a Brazilian population were randomly allocated into an experimental group receiving mechanical treatment and antibiotics, and a control group receiving mechanical treatment and placebo. Clinical and radiographic assessments, as well as microbiologic sampling for Actinobacillus actinomycetemcomitans, were performed at baseline and one year after the end of the treatment. At the termination of the study A. actinomycetemcomitans could be isolated from the oral cavity of all patients in the control group who harbored the bacterium at baseline and in 4 out of 8 patients in the experimental group. Both treatment modalities resulted in significant benefit on an individual basis. The experimental group, however, displayed better results than did the control group regarding gingival index (GI), probing depth (PD), clinical attachment level (CAL), and radiographic analysis of crestal alveolar bone mass, but not with respect to plaque index (PI). No serious adverse effects of the antibiotic treatment were observed in the present study.

Localized juvenile periodontitis and Actinobacillus actinomycetemcomitans in a Brazilian population.

Localized juvenile periodontitis (LJP) has been used as a model for studying periodontal disease, and its prevalence is considered to be higher in third-world countries (0.3-8%) than in industrialized countries (0.1%). Mostly, the disease has been associated with Actinobacillus actinomycetemcomitans (A.a.) but lack of association has also been reported. The aim of this study was to identify LJP patients in geographically different Brazilian populations and assess the presence of A.a. in their periodontal lesions. 7843 children, 12-19-years of age, from the cities of Rio de Janeiro, Votorantim and Belo Horizonte were screened, and LJP patients were identified by strict clinical and radiographical criteria. A final LJP prevalence of 0.3%, with a 99% confidence interval between 0.16% to 0.47%, was found. The prevalence in the subpopulations varied between 0.1-1.1% in the different areas. Subgingival bacterial samples were obtained from the oral cavity of 25 patients and their family members. 80% of these patients, 39.5% of their family members, 35.3% of their parents, and 43.9% of all siblings were culture positive for A.a. All but one of the families had at least one member in addition to the patient who was culture positive for A.a. In 3 families, > 1 member showed radiographic and clinical signs of LJP. 30% of non-LJP subjects coming from one of the areas with higher LJP prevalence harbored A.a. We conclude that LJP is highly associated with A.a. in this Brazilian population.

Attachment loss and serum antibody levels against autologous and reference strains of Actinobacillus actinomycetemcomitans in untreated localized juvenile periodontitis patients.

Immunological data have been suggested to be a potential tool in the diagnosis, classification and monitoring of periodontal diseases. However, the role of circulating antibodies in periodontal patients is poorly understood. Patients suffering from localized juvenile periodontitis (LJP) are often reported to show high titers of serum IgG antibodies against Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans), but several affected patients do not. Most studies use well-known reference strains of the bacterium for testing against the patients' sera. The aim of the present investigation was to study the relationship between serum IgG antibody levels to autologous A. actinomycetemcomitans strains and clinical attachment loss (CAL). In addition, we wanted to assess the patients' serum titers against 4 well-known reference strains of the bacterium as well as their general potential immunoglobulin response. Intravenous blood samples were taken from 23 LJP patients and 10 healthy individuals, and autologous A. actinomycetemcomitans strains were cultured from 18 of the LJP patients. CAL was measured at 4 different sites around all present teeth and assessed as a % of teeth with at least 1 site moderately > or = 2 < 5 mm) or severely (> or = 5 mm) involved. An enzyme-linked immunosorbent assay (ELISA) was performed to evaluate the serum titers of IgG antibodies to A. actinomycetemcomitans antigens. No significant correlation was found between serum IgG antibody titers to autologous strains and CAL. However, there was a trend that low responders had more moderately affected teeth than had high responders and patients with undetectable A. actinomycetemcomitans levels, which is in agreement with a hypothetically protective role of the antibodies. The total counts of immunoglobulin assessed in all participants showed that the predominant class was IgG and the reference group displayed significantly less (p < 0.05) IgG and IgG1 counts than the LJP patients. Both the reaction pattern against reference and autologous strains varied widely. We conclude that the specific antibody response against A. actinomycetemcomitans shows a weak correlation to clinical attachment levels in LJP patients.

Emotional stress effects on immunity, gingivitis and periodontitis.

Gingivitis and periodontitis are thought to result from an imbalance between those oral microorganisms which normally colonize tooth surfaces in close contact with the gingival margin, and the nature and efficiency of the host response. The bacteria are the triggering agents, but host defence mechanisms within the gingival/periodontal tissues seem to be responsible for most of the tissue damage and for the outcome and progression of the diseases. It has recently been shown that emotional or psychological load (stress) may influence immune activities directly via nerve messenger substances (neurotransmitters and neuropeptides) and/or indirectly via neuroendocrine (hormone) substances. This review discusses how emotional stressors and nervous and neuroendocrine responses to psychological stressors may modulate the immune response to bacteria, and thus be expected to influence the progression and course of gingivitis and periodontitis.

Bone density changes after 1 year in periodontal lesions treated surgically with or without ePTFE membrane placement.

The present study was designed to quantitatively assess radiographic changes in alveolar bone density in intrabony defects treated with expanded polytetrafluorethylene membranes (ePTFE) or by conventional flap surgery alone. 15 patients with 2 periodontal defects of comparable morphology which could be depicted on a single radiograph made up the test panel. Standardized radiographs of the periodontal defects were taken immediately prior to surgery and 12 months later. The 2 defects were treated simultaneously using the modified Widman flap procedure and prepared for membrane placement. Then one of the lesions was randomly assigned for treatment with the membrane. All radiographs and surgical procedures were managed by one person. The radiographs were assessed by another person according to a blind design. Periodontal defects treated with ePTFE membranes (test), and sites treated by conventional flap procedures (control) were then analyzed using a computerized image analysis program. In 8 patients, the test site outcome was better than the outcome in the control site. 6 of the control sites indicated increased bone density, while 7 sites showed decreased values, and 2 sites were unchanged. The corresponding values from the test sites were 5, 6 and 4, respectively. In the present controlled clinical study, the use of an ePTFE membrane to cover the opening of a vertical bone defects during periodontal surgery did not predictably increase the bone density of the defects.