Calprotectin levels in gingival crevicular fluid predict disease activity in patients treated for generalized aggressive periodontitis.

BACKGROUND AND OBJECTIVE: Clinical parameters such as probing depth and bleeding on probing are commonly used for monitoring after periodontal treatment. However, these parameters have poor prognostic utility. The biomarker calprotectin is used to monitor conditions such as inflammatory bowel disease because of its ability to predict disease activity. Levels of calprotectin in gingival crevicular fluid correlate with periodontal disease severity and treatment outcome. The validity of calprotectin as predictor for future periodontal disease activity has not yet been investigated. MATERIAL AND METHODS: Thirty-six subjects with generalized aggressive periodontitis were treated with scaling and root planing (SRP), and with adjunctive antimicrobial medications. Probing depth, clinical attachment level and bleeding on probing were assessed at baseline, and 3 and 6mo after SRP. A gingival crevicular fluid sample was collected from the initially deepest site in each patient 3mo after SRP and analysed for calprotectin levels. Activity was defined as a probing depth increase of >0.5mm between 3 and 6mo at the sample site. The ability of individual parameters to predict activity was analysed by construction of receiver operating characteristic curves. RESULTS: Nine active sites were identified. Clinical attachment level, probing depth, bleeding on probing and gingival crevicular fluid volume showed no predictive utility [area under the curve (AUC) <0.6, p>0.05]. However, calprotectin concentration (AUC=0.793, p=0.01) and the total amount/sample of calprotectin (AUC=0.776, p=0.02) significantly predicted activity. Patients with calprotectin levels above calculated cut-off values had significantly more active sites than patients with negative results. CONCLUSION: Calprotectin levels were predictors of disease activity at both site and subject levels. The calculated cut-off values provide a dichotomous basis for prospective evaluation of calprotectin as a diagnostic marker for monitoring periodontal treatment.

Induced apoptosis of chondrocytes by Porphyromonas gingivalis as a possible pathway for cartilage loss in rheumatoid arthritis.

The role of bacterial infections in the pathogenesis of rheumatoid arthritis (RA) has gained increasing interest. Patients with RA often exhibit periodontal disease, which is associated with pathogens like Porphyromonas gingivalis. The present study examines the direct effects of P. gingivalis on apoptosis of human chondrocytes (a feature of inflammatory joint diseases) as one can assume an interrelation of pathogenesis of RA and P. gingivalis infections. Primary chondrocytes were infected with P. gingivalis. Early apoptotic and dead cell analysis was performed using Annexin-V, 7AAD, and propidium iodide and examined by flow cytometry and fluorescence microscopy. Caspase activation and DNA fragmentation were determined by western blot analysis and TUNEL reaction. Flow cytometry and fluorescence microscopy demonstrated an increase of Annexin-V-positive early apoptotic chondrocytes after infection. Western blot showed upregulation of activated caspase-3 expression, and TUNEL reaction revealed considerable DNA fragmentation following infection. The data show that P. gingivalis promotes early and later stages of apoptosis of primary human chondrocytes, which might contribute to the joint damage seen in the pathogenesis of RA.

Periodontal disease in patients with ankylosing spondylitis.

OBJECTIVE: Ankylosing spondylitis (AS) and periodontal disease (PD) are characterised by dysregulation of the host inflammatory response, resulting in soft and hard connective tissue destruction. AS has been related to other inflammatory diseases, however, there is a paucity of data on whether AS is associated with inflammatory PD. METHODS: The association between AS and PD was examined in 48 patients with AS and 48 healthy controls, matched for age and gender. AS was diagnosed according to the modified New York criteria. Periodontal examination included probing pocket depth (PPD), clinical attachment loss (CAL), plaque index (PI) and bleeding on probing (BOP). Potential risk factors of PD such as smoking, low education, alcohol consumption, body mass index (BMI), as well as chronic diseases associated with PD and AS were assessed through questionnaires. RESULTS: In stepwise logistic regression, including AS status, age, gender, education, smoking, alcohol consumption and BMI, only AS status, age and education remained significant predictors of PD. Patients with AS had significant 6.81-fold increased odds (95% CI 1.96 to 23.67) of PD (defined as mean attachment loss >3 mm) compared to controls. The strength of the association was attenuated but remained statistically significant after further adjustment for plaque accumulation (odds ratio (OR) 5.48, 95% CI 1.37 to 22.00). CONCLUSIONS: The present study shows that patients with AS have a significantly higher risk of PD, strongly suggesting the need for close collaboration between rheumatologists, periodontists and dental hygienists when treating patients with AS.

Lysyl oxidase (lox) gene deficiency affects osteoblastic phenotype.

Lysyl oxidase (LOX) catalyzes cross-linking of elastin and collagen, which is essential for the structural integrity and function of bone tissue. The present study examined the role of Lox gene deficiency for the osteoblast phenotype in primary calvarial osteoblasts from E18.5 Lox knockout (Lox ( -/- )) and wild type (wt) (C57BL/6) mice. Next to Lox gene depletion, mRNA expression of Lox isoforms, LOXL1-4, was significantly downregulated in Lox ( -/- ) bone tissue. A significant decrease of DNA synthesis of Lox ( -/- ) osteoblasts compared to wt was found. Early stages of osteoblastic apoptosis studied by annexin-V binding as well as later stages of DNA fragmentation were not affected. However, mineral nodule formation and osteoblastic differentiation were markedly decreased, as revealed by significant downregulation of osteoblastic markers, type I collagen, bone sialoprotein, and Runx2/Cbfa1.

Effects of Porphyromonas gingivalis on cell cycle progression and apoptosis of primary human chondrocytes.

BACKGROUND: It has been suggested that bacterial infections have a role in the pathogenesis of rheumatoid arthritis (RA). P gingivalis, a Gram-negative, anaerobic rod, is one of the major pathogens associated with periodontal disease. OBJECTIVE: To examine P gingivalis infection and its effects on cell cycle progression and apoptosis of human articular chondrocytes. METHODS: Primary human chondrocytes cultured in monolayers were challenged with P gingivalis. Infection and invasion of P gingivalis into chondrocytes was analysed by scanning electron microscopy, double immunofluorescence and by antibiotic protection and invasion assay. Cell cycle progression of infected chondrocytes was evaluated by flow cytometry. Also, cell apoptosis was visualised by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) of DNA strand breaks and by western blot analysis. RESULTS: Data showed that P gingivalis could adhere and infect primary human chondrocytes. After chondrocyte infection, intracellular localisation of P gingivalis was noted. Flow cytometry analyses demonstrated affected cell cycle progression, with an increase of the G(1) phase and a significant decrease of the G(2) phase after infection. In addition, increased apoptosis of P gingivalis-infected chondrocytes was visualised by TUNEL assay and by upregulation of caspase-3 protein expression. CONCLUSION: These data demonstrate that P gingivalis infects primary human chondrocytes and affects cellular responses, which might contribute to the tissue damage seen in the pathogenesis of rheumatoid arthritis.

Association among rheumatoid arthritis, oral hygiene, and periodontitis.

BACKGROUND: A limited number of studies suggest a higher prevalence of periodontal disease among individuals with rheumatoid arthritis (RA); however, results have been inconsistent. Further, it is unclear to what extent poor oral hygiene among patients with RA may account for this association. METHODS: The association between RA and periodontitis was examined in 57 subjects with RA and 52 healthy controls, matched by age and gender. Oral examination included plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment loss (CAL). Potential risk factors for periodontal disease, such as smoking, education, alcohol consumption, and body mass index (BMI), as well as chronic diseases associated with RA and periodontal disease were assessed through questionnaires. RESULTS: In a stepwise logistic regression, including RA status, age, gender, education, smoking, alcohol consumption, and BMI, only RA status and age remained significant predictors of periodontal disease. Subjects with RA had a significant 8.05-fold increased odds (95% confidence interval: 2.93 to 22.09) of periodontitis compared to controls. The strength of the association was attenuated but remained statistically significant after further adjustment for PI, GI, or both. PI alone accounted for 12.4%, GI alone accounted for 11.1%, and PI and GI combined accounted for 13.4% of the association between RA and periodontitis. CONCLUSIONS: Subjects with RA have significantly increased periodontal attachment loss compared to controls. Oral hygiene may only partially account for this association.

Clinical and inflammatory effects of galvano-ceramic and metal-ceramic crowns on periodontal tissues.

Prosthetic crowns made by galvano-forming are considered to be highly biocompatible and aesthetic restorations. Therefore, they represent an alternative crown-system to conventional metal-ceramic crowns in replacing lost tooth structure. However, there are few data available on clinical and biochemical effects of galvano-ceramic crowns on periodontal tissues. The purpose of this controlled study was to test the impact of galvano-ceramic crowns and metal-ceramic crowns on clinical and inflammatory responses of periodontal tissues. A prospective, blinded randomized clinical trial was conducted. Galvano-ceramic crowns and metal-ceramic crowns were placed in 52 periodontally healthy patients in split-mouth design. Clinical parameters (gingival index, plaque index, probing depths and recessions) were recorded from six sites per tooth. Initial tissue alteration was accessed analysing the gingival crevicular fluid flow rate and IgG concentration in gingival crevicular fluid. After 24 months, 34 patients could be re-evaluated. All crowns were in adequate function and obvious clinical inflammation was rarely observed. After 24 months of follow-up, gingival tissues adjacent to galvano-ceramic crowns showed significantly less signs of clinical and inflammatory responses according to plaque index (P = 0.004), gingival index (P < 0.001), gingival crevicular fluid flow rate (P = 0.012) and IgG (P = 0.002). Data were also analyzed for buccal and oral sites separately. Gingival tissues adjacent to metal-ceramic crowns showed significantly increased clinical and inflammatory values for plaque index (P = 0.005), gingival index (P = 0.008), gingival crevicular fluid flow rate (P = 0.006), IgG (P = 0.007) at oral sites compared to galvano-ceramic crowns. Our data suggest a stabilizing effect of galvano-ceramic crowns on periodontal tissues over time.

Prediction of periodontal disease from multiple self-reported items in a German practice-based sample.

BACKGROUND: Ascertainment of periodontal disease using self-reported measures would be useful for large epidemiologic studies. This study evaluates whether a combination of self-reported items with established risk factors in a predictive model can assess periodontal disease accurately. METHODS: Responses of 246 subjects to a detailed questionnaire were compared to their periodontal disease history as assessed from radiographs. Multiple regression modeling was used to construct predictive models using self-reported items and established risk factors. RESULTS: Depending on the definition of gold-standard periodontal disease, two or three self-reported items were selected for the predictive models, in addition to age, gender, and smoking. Self-reported tooth mobility was associated strongly with periodontal disease independent of other risk factors and was selected in all models. For dichotomous definitions of periodontal disease, discrimination of predictive logistic regression models was good with areas under the receiver operating characteristic curve >0.80. Assessment of periodontal disease history based on extreme quantiles of model-predicted values yielded high sensitivity and specificity. CONCLUSION: The combination of several self-reported items may be useful for ascertainment of periodontal disease in epidemiologic studies.

Porphyromonas gingivalis dihydroceramides induce apoptosis in endothelial cells.

Porphyromonas gingivalis dihydroceramides are found in extracts of calculus-contaminated root surfaces, diseased gingival tissue, and atherosclerotic plaques. These ceramides have been shown to promote inflammatory secretory responses in gingival fibroblasts. Little is known about their effects on the vascular system. We tested the hypothesis that P. gingivalis lipids induce apoptosis of human endothelial cells, and investigated the effects of extracted and purified P. gingivalis lipids on human umbilical vein endothelial cells. P. gingivalis phosphoglycerol dihydroceramides induced apoptosis, but not necrosis, in endothelial cells. Early apoptotic cells showed exposure of phosphatidylserine on the cell surface, followed by the cleavage of procaspases 3, 6, and 9. The release of apoptosis-inducing factor was increased, suggesting mitochondrial involvement. Different caspase inhibitors and cAMP elevation blocked DNA fragmentation. Moreover, N-acetylcysteine significantly reduced apoptosis, suggesting a role for reactive oxygen species in this process. Analysis of these data indicates that dihydroceramides may be important virulence factors of P. gingivalis.

Obesity, inflammation, and periodontal disease.

The prevalence of obesity has increased substantially over the past decades in most industrialized countries. Obesity is a systemic disease that predisposes to a variety of co-morbidities and complications that affect overall health. Cross-sectional studies suggest that obesity is also associated with oral diseases, particularly periodontal disease, and prospective studies suggest that periodontitis may be related to cardiovascular disease. The possible causal relationship between obesity and periodontitis and potential underlying biological mechanisms remain to be established; however, the adipose tissue actively secretes a variety of cytokines and hormones that are involved in inflammatory processes, pointing toward similar pathways involved in the pathophysiology of obesity, periodontitis, and related inflammatory diseases. We provide an overview of the definition and assessment of obesity and of related chronic diseases and complications that may be important in the periodontist's office. Studies that have examined the association between obesity and periodontitis are reviewed, and adipose-tissue-derived hormones and cytokines that are involved in inflammatory processes and their relationship to periodontitis are discussed. Our aim is to raise the periodontist's awareness when treating obese individuals.

Prediction of Periodontal Disease From Multiple Self-Reported Items in a German Practice-Based Sample.

BACKGROUND: Ascertainment of periodontal disease using self-reported measures would be useful for large epidemiologic studies. This study evaluates whether a combination of self-reported items with established risk factors in a predictive model can assess periodontal disease accurately. METHODS: Responses of 246 subjects to a detailed questionnaire were compared to their periodontal disease history as assessed from radiographs. Multiple regression modeling was used to construct predictive models using self-reported items and established risk factors. RESULTS: Depending on the definition of gold-standard periodontal disease, two or three self-reported items were selected for the predictive models, in addition to age, gender, and smoking. Self-reported tooth mobility was associated strongly with periodontal disease independent of other risk factors and was selected in all models. For dichotomous definitions of periodontal disease, discrimination of predictive logistic regression models was good with areas under the receiver operating characteristic curve >0.80. Assessment of periodontal disease history based on extreme quantiles of model-predicted values yielded high sensitivity and specificity. CONCLUSION: The combination of several self-reported items may be useful for ascertainment of periodontal disease in epidemiologic studies.

Recent concepts in plaque formation.

Dental plaque is an adherent, bacterial film, and is the main pathological agent for periodontal diseases. The formation of dental plaque can occur both supragingivally and subgingivally. The development of plaque is a three-step process. Following the formation of a pellicle, pioneer micro-organisms will adhere to it, proliferate and form colonies. The final stage involves the aggregation of filamentous organisms and spirochetes into a cohesive biofilm. Many products of the plaque bacteria reach the subepithelial tissue, causing inflammatory responses such as increased vascularity and leukocyte diapedesis. Both supragingival and subgingival plaque may form a hard, mineralized mass called calculus. The surface of calculus harbours bacteria, which may exacerbate the inflammatory responses. An effective oral antiseptic must be active against a wide range of Gram-positive and Gram-negative bacterial species, including streptococci and fusobacteria. Ideally, an effective agent would also penetrate the plaque biofilm. Data show that essential oil and chlorhexidine mouthwashes have the broadest antimicrobial effects.

Salivary IgA subclasses and bacteria-reactive IgA in patients with aggressive periodontitis.

The local salivary immunoglobulin A (IgA) response in patients with aggressive periodontitis to oral microorganisms and its role for the pathogenesis has not been determined. This study investigated the hypothesis that aggressive periodontitis patients have impaired oral secretory immunity. Our test group was made-up of 19 aggressive periodontitis patients and 19 age- and gender-matched periodontally healthy controls. Total IgA, IgA subclass 1, IgA subclass 2 and IgA reactive to Actinobacillus actinomycetemcomitans Y4, Treponema denticola ATCC 35404 and Candida albicans DSM 3454 were determined by enzyme-linked immunosorbent assay in whole unstimulated and stimulated saliva. A statistically significantly lower concentration and secretion rate of total salivary IgA (P < 0.01) and IgA1 (P < 0.001) was found in the aggressive periodontitis group in resting and stimulated saliva. A decrease of IgA2 (P < 0.05) was seen in resting saliva. Although only minor differences were detected in the concentration and secretion of bacteria-reactive IgA in both groups, the proportion of bacteria-reactive IgA from the total IgA was significantly higher (P < 0.01) in the aggressive periodontitis group in all three microorganisms tested. Our results indicate an inhibition of total secretory IgA. In particular an IgA subclass 1-specific decrease in aggressive periodontitis was noted, while the bacteria-reactive humoral immune system in saliva was activated. The role of the decrease of IgA1 immunoglobulins in aggressive periodontitis with respect to susceptibility for periodontal diseases has to be elucidated.

Secretion of gelatinases and activation of gelatinase A (MMP-2) by human rheumatoid synovial fibroblasts.

In monolayer cultures human rheumatoid synovial fibroblasts (HRSF) secrete gelatinase A (MMP-2) and, unlike other human fibroblasts, to a minor extent also gelatinase B (MMP-9) as inactive proenzymes. In this regard HRSF resemble the fibrosarcoma cell line HT-1080. Unlike HT-1080, however, HRSF do not increase the secretion of MMP-9 in response to phorbol-12-myristate-13-acetate. This indicates that in HRSF the protein kinase C pathway for an enhanced MMP-9 secretion is inactive. None of the substances used in our study increased MMP-9 secretion, but some of them inhibited MMP-9 secretion. The secretion of MMP-2 could not be enhanced either, not even by dbcAMP, which has been reported to be effective in Sertoli and peritubular cells. Activation of MMP-2 in HRSF could be induced by treatment with concanavalin A (ConA) or cytochalasin D, as was shown for other cell types. This activation was not accompanied by a significant change in the amount of secreted TIMP-1 and TIMP-2. In contrast to reports on human skin fibroblasts, however, the activation of MMP-2 could not be induced in HRSF by treatment of the cells with monensin or sodium orthovanadate. Moreover, monensin was shown to act as an inhibitor of ConA- or cytochalasin D-mediated activation. Additionally, and in contrast to a report on a rat fibroblast cell line, MMP-2 activation is not mediated via the MAP kinase pathway in HRSF: PD 98059, a specific inhibitor of MAP kinase kinase, did not inhibit the activation of MMP-2. Similarly ineffective were PD 169316, an inhibitor for p38 MAP kinase, other inhibitors for protein kinases as lavendustin A, Gö 6983, wortmannin, rapamycin, as well as the protein tyrosine kinase inhibitors herbimycin A and genistein. Only staurosporin, a broad spectrum inhibitor of protein kinases, and the ionophores monensin and A 23187 effectively inhibited MMP-2 activation in HRSF. Our results demonstrate that MMP-2 can be activated by quite different pathways, and that different cells, even when belonging to the fibroblast family, do not necessarily use the same activating pathways.

Local versus systemic adjunctive antibiotic therapy in 28 patients with generalized aggressive periodontitis.

BACKGROUND: Although the use of systemic antibiotics has been studied in patients with generalized aggressive periodontitis (formerly rapidly progressive periodontitis), the use of adjunctive tetracycline fibers in these patients has not been reported. The purpose of the present study was to compare the clinical response of local versus systemic antibiotic treatment as adjuncts to scaling and root planing in patients with GAgP. METHODS: After initial therapy and full-mouth scaling and root planing (SRP), 30 patients were randomly assigned to 1 of 2 antibiotic treatment groups. Probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BOP) were recorded with an automated probe prior to SRP at baseline (BL) and 15, 30, 41, and 54 weeks later. Three months after SRP, the patients were treated with amoxicillin/clavulanic acid (500 mg tid; SRP + AUG group) or with local tetracycline fiber in pockets with PD > or =5 mm (SRP + TCF group). RESULTS: In both treatment groups, PD decreased significantly from BL to week 54 (6.2+/-1.5 mm to 4.7+/-1.4 mm for SRP + TCF and 6.5+/-1.4 mm to 4.2+/-0.6 mm for SRP + AUG). However, there was no statistically significant difference between the 2 groups in pocket reduction. Similarly, in both treatment groups, there were small but significant gains in CAL from BL to week 54 (12.0+/-1.8 mm to 11.3+/-1.8 mm for SRP + TCF and 12.3+/-1.5 mm to 11.2+/-1.2 mm for SRP + AUG). The difference in CAL gain between the 2 groups was not statistically significant. At the final examination, both groups showed significant PD reduction and CAL gain (P <0.001) compared to BL. The frequency and percentage of bleeding sites decreased significantly in both groups. At week 54, this decrease was significantly greater in the SRP + AUG group (31.67% for SRP + TCF versus 3.85% for SRP + AUG). CONCLUSIONS: These results indicate that the local delivery of tetracycline by a fiber or the systemic administration of amoxicillin/clavulanic acid given 3 months after scaling and root planing produced similar clinical outcomes over the 9-month observation period.

Observations on a new collagen barrier membrane in 16 consecutively treated patients. Clinical and histological findings.

BACKGROUND: Space-maintaining capacity, cell disclusive potential, and stability over time are crucial factors to achieving sufficient bone augmentation with membrane barriers. The case series presented here assessed a new collagen barrier used in bone augmentation. Clinically, the healing pattern, especially in cases of secondary healing, was studied. METHODS: Soft tissue healing was documented by photographs, and the size of the dehiscences calculated by image analysis. The measurements were performed on digitized photographs. During reentry, barrier remnants were dissected and histologically evaluated. RESULTS: The mean value for dehiscences was 35.5 mm2; all dehiscences healed within 4 weeks after the exposure became evident. The difference was statistically significant between the week 2 and week 6 visits (P = 0.008) for each previously exposed site. The histologic observation of barrier remnants revealed direct apposition of fibrous and bone tissues on the membrane surface. CONCLUSION: In cases of membrane exposure, gingival dehiscences always disappeared in the following weeks without affecting the healing process. Histologic results showed barrier stability over a 6-month period, promoting bone regeneration.

A novel technique for monitoring the development of bacterial biofilms in human periodontal pockets.

A new technique is presented for analyzing subgingival bacterial plaque. Different materials (polytetrafluoroethylene, gold, dentin) kept for several days in periodontal pockets of patients suffering from periodontitis were analyzed by electron microscopy and fluorescence in situ hybridization (FISH). Those parts of the carriers extending into the deepest zone of the pockets were predominantly colonized by spirochetes and Gram-negative bacteria whereas those segments in contact with a shallower region were colonized by streptococci. Independent of the material used, the bacterial colonization of the carriers appears to be similar. FISH using eubacteria- and species-specific oligonucleotides on semi-thin cross-sections of the carriers in combination with confocal laser scanning microscopy allowed detailed analysis of the architecture of biofilms and identification of putative periodontal pathogens with single cell resolution.

Total IgA and Porphyromonas gingivalis-reactive IgA in the saliva of patients with generalised early-onset periodontitis.

Generalised early-onset periodontitis (GEOP) is characterized by acute inflammatory bursts, resulting in rapid destruction of the periodontal apparatus in young adults. An impaired host defense seems to play an important role as etiological factor of periodontitis, especially in the development of GEOP. As the gram-negative Porphyromonas gingivalis has been identified as one of the causative anaerobic bacteria, the humoral immune response to this micro-organism is of particular interest in patients with GEOP. To evaluate the local immune status, we measured total and P. gingivalis-reactive salivary IgA in GEOP patients and in age- and gender-matched periodontally normal controls. We found a significantly lower concentration and secretion rate of total salivary IgA in the GEOP group. Although no differences were detected in the concentration or secretion of P. gingivalis-reactive IgA between groups, the specific fraction of P. gingivalis-reactive IgA of the total IgA was significantly higher in the GEOP group. These findings indicate an inhibition of total secretory IgA in GEOP, while the P. gingivalis-reactive humoral immune system in saliva is, however, activated. P. gingivalis seems to selectively activate IgA lymphocyte clones and induces a switch in the fraction of specific IgA.

Suppression of interleukin-10 release from human periodontal ligament cells by interleukin-1beta in vitro.

Periodontitis is characterized by an inflammatory process induced by periodontopathogenic bacteria in the subgingival plaque. Periodontal inflammation can be enhanced by both an increase of inflammatory stimulators, e.g. interleukin (IL)-6, and a decrease of inflammatory inhibitors, e.g. IL-10. The amount of IL-1beta is known to be increased in gingival tissues and in the gingival crevicular fluid from inflamed sites compared to healthy sites. This in vitro study sought to clarity whether IL-1beta (1 ng/ml) has a regulatory effect on the release of these two cytokines from human periodontal ligament (PDL) cells. PDL cells derived from healthy premolars were grown in the presence and absence (control) of IL-1beta. The concentration of IL-6 and IL-10 in the supernatants was assessed by enzyme-linked immunosorbent assay after 48 h of culture. PDL cells incubated with IL-1beta released significantly (p < 0.05) higher amounts of IL-6 and significantly (p < 0.01) smaller amounts of IL-10 compared to control. These results give further support to the observation that IL-1beta can increase the IL-6 secretion from PDL cells. Moreover, they provide original evidence that PDL cells secrete IL-10, which can be suppressed by IL-1beta. It is concluded that PDL cells can function as accessory immunoinflammatory cells amplifying the inflammatory process in periodontitis and, thereby, contributing to periodontal breakdown.

Repeated local metronidazole-therapy as adjunct to scaling and root planing in maintenance patients.

The purpose of this investigation was to evaluate the effect of local antibiotic therapy with metronidazole adjunctively to scaling and root planing (SRP) versus mechanical treatment alone. 30 maintenance-patients were included in this single-blind study. The subjects had to comply with the following criteria: 2 non-adjacent sites with a probing depth > or =6 mm with bleeding on probing in separate quadrants, no periodontal therapy within the last 3 months, and no antibiotic therapy within the last 6 months. After randomization, the study sites were assigned to one of the following 2 treatments: SRP plus subgingival application of metronidazole 25% dental gel (Elyzol) 5x during 10 days (test site) or SRP alone (control site). Subgingival microbiological samples were taken prior to, and 21 days and 3 months after scaling. The samples were analyzed with a commercial chair-side ELISA (Evalusite) for Porphyromonas gingivalis, Prevotella intermedia and Actinobacillus actinomycetemcomitans. Probing pocket depth (PPD), attachment level (AL) and bleeding on probing (BOP) were recorded at baseline and 3 months later. PPD reduction and AL-gain were statistically significant (p<0.001) after both treatments. However, there were no statistically significant differences between them. The same observation was made for BOP. P. gingivalis was reduced significantly after both treatments without statistically significant differences. P. intermedia was reduced significantly only after SRP. A. actinomycetemcomitans was not reduced significantly after either treatment. In conclusion, the repeated local application of metronidazole as an adjunct to SRP and the mechanical treatment alone showed similar clinical and microbiological effects without statistically significant differences with the exception of P. intermedia.