Analysis of galectin-3 levels as a source of coronary heart disease risk during periodontitis.

BACKGROUND AND OBJECTIVE: Different evidence has shown that Galectins have a key role as modulators of cell surface functions and signaling in a wide range of inflammatory diseases during their preclinical stages. The aim of this study was to analyze the association and impact of periodontitis and coronary heart disease (CHD) on salivary and serum Galectin-3 in patients with periodontitis and CHD. MATERIALS AND METHODS: For the present study, healthy controls (n = 38), periodontitis (n = 40), CHD (n = 39), and a combination of periodontitis +CHD (n = 38) patients were enrolled and analyzed. In each patient, demographic characteristics and a full-mouth clinical periodontal examination were achieved. Moreover, serum and salivary samples were collected to assess Galectin-3 and Endothelin-1 (ET-1) levels. The Jonckheere-Terpstra p-trend and Spearman's correlation tests as well as uni- and linear regression analyses were used to analyze the study data. RESULTS: Patients with periodontitis (serum, p = .003; saliva, p < .001) and periodontitis + CHD groups (serum p = .004; saliva, p < .001) had higher median serum and salivary concentrations of Galectin-3 in comparison with CHD and healthy controls. Serum (p = .006) and salivary (p = .009) Galectin-3 levels were significantly correlated with serum ET-1. The multivariate regression analysis highlighted that periodontitis (p = .047) was the significant predictor of serum Galectin-3 levels while ET-1 (p = .028) was the significant predictor of salivary Galectin-3 levels. CONCLUSION: The results showed that patients with periodontitis and periodontitis + CHD presented significant higher serum and salivary Galectin-3 levels in comparison with CHD patients and healthy subjects. Periodontitis and ET-1 were the significant predictors of serum and salivary Galectin-3 levels, respectively.

Association of vitamin D in patients with periodontitis: A cross-sectional study.

BACKGROUND AND OBJECTIVE: Vitamin D has been considered to possess anti-inflammatory and antimicrobial activity, which may be a link for the known interaction of periodontitis (CP) and coronary heart disease (CHD). This study investigated the association between serum vitamin D levels and periodontitis in patients with CP and with CHD. Furthermore, the objective was to determine whether periodontitis and CHD had an impact on serum vitamin D levels. MATERIAL AND METHODS: Using a cross-sectional design, a total of 46 patients with CP, 45 patients with CHD, 45 patients with both CP and CHD, and 43 healthy patients were enrolled in the present study. RESULTS: Patients in the CP (17.4 ± 5.2 ng/mL) and in the CP + CHD (16.5 ± 5.6 ng/mL) group presented a significantly lower mean serum level of 25(OH)vitamin D compared to patients in the CHD (24.6 ± 3.7 ng/mL) and healthy control groups (29.9 ± 5.4 ng/mL) (P < .001). 25(OH)vitamin D levels were positively correlated with the number of teeth and negatively with C-reactive protein (CRP) and all periodontal parameters (P < .001). In all patients, there was a proportional increase of 25(OH)vitamin D levels with a progressive increase in number of teeth (P-trend <.001) while there were a proportional decrease in 25(OH)vitamin D levels with a progressive increase in clinical attachment level (CAL, P-trend = .001), probing depth (PD, P-trend = .006), and bleeding sites (BOP, P-trend <.001) levels. CONCLUSION: Patients with CP and CP + CHD presented significantly lower serum levels of vitamin D compared to CHD and healthy controls. Moreover, the presence of CP negatively influenced serum vitamin D levels.

The effects of a desiccant agent in the treatment of chronic periodontitis: a randomized, controlled clinical trial.

OBJECTIVE: Chemotherapeutic agents have been widely used as adjuncts for the treatment of chronic periodontitis (CP). This study investigated and compared a desiccant agent as an adjunct to scaling and root planing (SRP) versus SRP alone for the treatment of CP. MATERIALS AND METHODS: Thirty-six patients with CP were studied. Using a split-mouth design, the maxillary right and left quadrants were randomly assigned to SRP plus desiccant (Hybenx® EPIEN Medical, Inc. St. Paul, MN, USA) or SRP alone. Patients were examined on a regular basis for clinical, microbiological, and inflammatory mediator changes over a 1-year period. Clinical attachment level (CAL) was the primary outcome variable. In addition, the red complex bacteria and gingival crevicular fluid (GCF) inflammatory mediators were monitored. RESULTS: Compared to baseline, both treatments demonstrated an improvement in periodontal parameters. Compared to SRP alone, SRP plus desiccant yielded a significant improvement in probing depth (PD) (SRP: 2.23 ± 0.31 mm vs. desiccant: 3.25 ± 0.57 mm, p < 0.05), CAL (SRP: 3.16 ± 0.29 mm vs. desiccant: 4.21 ± 0.34 mm, p < 0.05 mm) and bleeding on probing (BOP) (SRP: 4.56 ± 1.5% vs. desiccant: 34.23 ± 4.2%, p < 0.001) at 12 months. Similarly, in the SRP plus desiccant group, the bacteria of the red complex were significantly reduced (p < 0.05); and the level of inflammatory mediators was significantly reduced (p < 0.003) compared to SRP alone. CONCLUSIONS: SRP plus the desiccant resulted in a greater reduction in clinical, microbial and inflammatory mediators compared to SRP alone. CLINICAL RELEVANCE: Desiccant, when combined to SRP, was demonstrated as a significant approach to control the levels of certain periodontal pathogens, inflammatory mediators in patients with CP.

Accelerated orthodontic tooth movement: molecular mechanisms.

Accelerating orthodontic tooth movement can significantly reduce treatment duration and risks of side effects. The rate of orthodontic tooth movement is chiefly determined by the remodeling of tissues surrounding the roots; this in turn is under the control of molecular mechanisms regulating cellular behaviors in the alveolar bone and periodontal ligament. This review summarizes the current knowledge on the molecular mechanisms underlying accelerated orthodontic tooth movement, and the clinical and experimental methods that accelerate orthodontic tooth movement with possible molecular mechanisms. The review also shows directions for future studies to develop more clinically applicable methods to accelerate orthodontic tooth movement.

Impact of N-terminal pro-B-type natriuretic peptide and related inflammatory biomarkers on periodontal treatment outcomes in patients with periodontitis: An explorative human randomized-controlled clinical trial.

BACKGROUND: N-terminal portion of the B-type natriuretic propeptide (NT-proBNP) has potentially been shown to play an important role in the development of periodontitis and cardiovascular disease (CVD). This study evaluated the efficacy of periodontal treatment on NT-proBNP and related CVD biomarkers and explored whether subjects harboring high NT-proBNP at baseline showed increased clinical benefits with the non-surgical periodontal treatment performed with full-mouth scaling and root planing (FM-SRP) at 6-month follow-up. METHODS: Forty-eight patients with stage III periodontitis were randomized to receive minimal standard oral care (SOC) (n = 24) or FM-SRP (n = 24) protocol. Clinical periodontal parameters (probing depth, clinical attachment loss, bleeding on probing), serum NT-proBNP, α1-antitrypsin, C-reactive protein (hs-CRP), endothelial cell-specific molecule-1 (ECM-1), and neutrophil gelatinase-associated lipocalin (NGAL) concentrations were assessed at baseline and at 1-, 3-, and 6- month follow-up. RESULTS: At 6 months, FM-SRP was more effective than SOC in reducing periodontal parameters and mean proportions of NT-proBNP (p = 0.004), hs-CRP (p = 0.003), α1-antitrypsin (p = 0.012), ECM-1 (p = 0.014), and NGAL (p = 0.045). At 6-month follow-up, the reduced NT-proBNP, α1-antitrypsin, hs-CRP, ECM-1, and NGAL levels were significantly correlated with the extent of periodontitis (p < 0.05). Furthermore, the analysis of variance analysis evidenced that, at 6-month follow-up, FM-SRP significantly impacted the reduction of NT-proBNP, hs-CRP, ECM-1, and NGAL. Moreover, high levels of NT-proBNP, hs-CRP, ECM-1, and NGAL at baseline significantly influenced the efficacy of periodontal treatment positively. CONCLUSION: In this study, FM-SRP was more effective than SOC in reducing clinical variables and NT-proBNP levels, although subjects who harbored high NT-proBNP concentrations at baseline showed greater clinical benefits of periodontal treatment at 6-month follow-up.

Oro-facial manifestations in patients with eating disorders.

Studies have reported that the oral health status is jeopardized in patients with eating disorders. The aim was to review the oro-facial manifestations in patients with eating disorders. The address the focused question was "What is the oro-dental health status in patients with eating disorders?" MEDLINE/PubMed and Google Scholar databases were searched from 1948 to March 2012 using the following terms in various combinations: "Anorexia nervosa", "bulimia nervosa", "eating disorders", "dental", "oral health status". Letters to the editor, unpublished data and articles published in languages other than English were excluded. Dry lips, burning tongue and parotid gland swelling are common manifestations in patients with eating disorders as compared to medically healthy controls. The association of dental caries and periodontal disease in patients with eating disorders remains debatable. Temporomandibular disorders have also been reported to be more prevalent in patients with eating disorders as compared to healthy controls. A critical oral-dental examination during routine dental check-ups may reveal valuable information regarding the presence or absence of eating disorders in routine dental patients. This may be important information, updating the medical history, supporting the role of the physician.

Effect of an herbal mouth rinse in preventing periodontal inflammation in an experimental gingivitis model: a pilot study.

BACKGROUND: Gingivitis is a chronic inflammatory condition, resulting from gingival bacteria and bacterial byproducts. Antiplaque oral rinses reduce inflammation by removing or inhibiting plaque formation. The purpose of this pilot study was to examine the anti-inflammatory effects of HM-302, a mouth rinse based on natural products, on gingival inflammation. METHODS: A prospective, double-blinded, randomized parallel-group controlled trial involving 62 patients was conducted to assess efficacy and safety. During a 2-week period with no dental hygiene, subjects were randomized to receive either the study rinse (HM-302); a cetylpyridinium chloride (CPC) rinse; an essential oils (EO) rinse; or a water-only preparation. The gingival index (GI), plaque index (PI), and number of bleeding sites were measured at baseline and at the end of the study period. RESULTS: Progression of gingival inflammation resulting from lack of dental hygiene was lowest in patients treated with the HM-302 rinse, and was significantly less marked than in patients treated with the water-only preparation. When compared to the CPC and EO treatments, HM-302 was the only mouth rinse that was significantlybetter than the control, with respect to both the change in absolute GI scores (p = .006) and to the percent increase in GI scores (p = .012). No serious adverse effects were noted in any of the study groups. CONCLUSION: HM-302 is a safe and effective treatment for preventing the development of gingival inflammation in an experimental gingivitis model. Further research is needed to evaluate its long-term effects.

Periodontitis activates the NLRP3 inflammasome in serum and saliva.

BACKGROUND: Nod-like receptor family pyrin domain-containing protein-3 (NLRP3) complex inflammasome has potentially been shown to play an important role in the development of periodontitis and diabetes. The objective of this study was to analyze the association between serum and salivary NLRP3 concentrations in patients with periodontitis and type-II diabetes mellitus (DM) and to evaluate whether this association was influenced by potential confounders. METHODS: For the present study, a cohort of healthy controls (n = 32), and patients with periodontitis (n = 34), type-II DM (n = 33), and a combination of periodontitis + type-II DM (n = 34) were enrolled. Patients were characterized on the basis of their periodontal status and analyzed for demographic characteristics, serum mediators, and for serum and salivary concentrations of NLRP3. A uni- and multivariate model was established to analyze whether periodontitis, type-II DM, and CRP influenced serum and salivary NLRP3 concentrations. RESULTS: In comparison to type-II DM patients and healthy controls, patients with periodontitis (serum, P = 0.003; saliva P = 0.012) and periodontitis + type-II DM (serum, P = 0.028; saliva, P = 0.003) had elevated serum and salivary NLRP3 concentrations. The multivariate regression model showed that periodontitis (P = 0.029) and HDL-cholesterol (P = 0.012) were significant predictors of serum NLRP3 concentrations whereas periodontitis (P = 0.036) and CRP (P = 0.012) were significant predictors of salivary NLRP3. CONCLUSION: The results of the present study showed that periodontitis and periodontitis + type-II DM patients had higher serum and salivary NLRP3 concentrations in comparison to healthy controls and patients with type-II DM. Periodontitis was demonstrated to be a significant predictor of both serum and salivary NLRP3 concentrations.

Independent impact of periodontitis and cardiovascular disease on elevated soluble urokinase-type plasminogen activator receptor (suPAR) levels.

BACKGROUND: Previous studies have demonstrated that a soluble urokinase-type plasminogen activator receptor (suPAR) plays an essential function in leukocytes and endothelial homeostasis and, therefore, in the development of coronary heart disease (CHD) and periodontitis. The aim of this study was to analyze the impact of gingival health, periodontitis, and CHD on suPAR levels in plasma and saliva and to evaluate suPAR as a biomarker of periodontitis and CHD. METHODS: Healthy controls (n = 33), patients with periodontitis (n = 31), CHD (n = 29), and a combination of periodontitis + CHD (n = 29) were enrolled in the present study. All patients were clinically and periodontally evaluated and regularly assessed for socioeconomic status, serum lipids, high-sensitivity C-reactive protein (hs-CRP), and for plasma and salivary suPAR levels. RESULTS: Patients with periodontitis (P <.001) and with periodontitis + CHD (P <.001) presented higher median plasma and salivary suPAR levels compared with CHD and healthy controls. Moreover, univariate regression analysis demonstrated that hs-CRP (P <.001) and periodontitis (P <.001) had a significant negative direct effect on both plasma and salivary suPAR levels. The multivariate regression analysis showed that periodontitis was the only significant predictor of plasma suPAR (P = .035) while hs-CRP was the only significant predictor of salivary suPAR (P <.001). CONCLUSIONS: The results of the present study demonstrated that patients with periodontitis and periodontitis + CHD presented higher suPAR levels in both plasma and saliva in comparison with healthy controls and CHD. Moreover, periodontitis and hs-CRP were the only significant predictors of the augmented suPAR levels in plasma and saliva, respectively.

New directions in host modulation for the management of periodontal disease.

BACKGROUND: New strategies for periodontal disease management have been emerging as more is learned about the role of the host response. Our increasing understanding of inflammation and its resolution has opened the door to the study of new periodontal treatment strategies. This commentary examines periodontal disease in light of a new understanding of the role of inflammation in disease expression, thus setting the stage for the development of new prevention and treatment strategies of a widespread disease. METHODS: We examined current publications and focused on articles relating to anti-inflammatory and pro-resolution mechanisms in periodontal disease. RESULTS: Recent research has examined the inflammatory and resolution cascade in greater detail while looking at endogenous and exogenous mediators that can be utilized to achieve therapeutic end-points. The possible introduction of "resolution indices" for drug testing warrants a new look at pharmacologic agents that might have been overlooked for their beneficial effects in periodontal disease treatment. CONCLUSION: The emerging awareness of inflammation and its control in periodontal disease management underscores the importance of exploring inflammatory pathways and mediators, thus exploring new ways to control inflammation. This direction of research promises a new era in drug discovery and therapeutics for periodontal disease treatment.

Modulation of the host inflammatory response in periodontal disease management: exciting new directions.

BACKGROUND: New strategies for periodontal disease management have been emerging as more is learned about the role of the host response. Our increasing understanding of inflammation and its resolution has opened the door to the study of new periodontal treatment strategies. This review examines periodontal disease in the light of a new understanding of the role of inflammation in disease expression thus setting the stage for the development of new prevention and treatment strategies of a widespread disease. METHODS: We examined current publications and focused on articles relating to anti-inflammatory and pro-resolution mechanisms in periodontal disease. RESULTS: Recent research has examined the inflammatory and resolution cascade in greater detail while looking at endogenous and exogenous mediators that can be utilised to achieve therapeutic end-points. The possible introduction of 'resolution indices' for drug testing warrants a new look at pharmacologic agents that might have been overlooked for their beneficial effects in periodontal disease treatment. CONCLUSION: The emerging awareness of inflammation and its control in periodontal disease management underscores the importance of exploring inflammatory pathways and mediators, thus exploring new ways to control inflammation. This direction of research promises a new era in drug discovery and therapeutics for periodontal disease treatment.

Understanding and managing periodontal diseases: a notable past, a promising future.

Throughout the 20th century, an understanding of the role of causative bacteria and the susceptible host in the initiation and progression of periodontal disease(s) has emerged from the research efforts of scientists and clinicians worldwide. Over time, specific bacterial types, such as Porphyromonas gingivalis, were discovered and shown to be important in the cause of periodontal disease. At the same time, inflammatory mediators, such as prostaglandins and interleukins, and enzymes, such as matrix metalloproteinases, were discovered and found to be important participants in the destruction of periodontal tissues. Acquired and inherited environmental risk factors began to emerge that could explain, in part, the susceptibility of individuals to periodontal disease. The discovery of antibiotics, beginning with sulfanilamide, penicillin, and streptomycin, led to additional strategies for managing periodontal disease. With the discovery of the mechanism of action of aspirin, scientists began to develop new strategies for treating diseases that focused on controlling inflammation. Thus, host-modulating therapies emerged for the management of periodontal disease through the control of inflammation. At the end of the 20th century, an old concept in medicine and dentistry reappeared: that the infection and inflammation of periodontal disease in the mouth could reach distant sites via the bloodstream. Apparently oral disease could, in fact, contribute to systemic diseases, such as atherosclerosis, diabetes, and adverse outcomes in pregnancy. This concept of the oral health-general health connection is now supported by sound and rational evidence-based observations. Clearly, the 21st century has arrived with a new understanding of the nature of periodontal diseases based on a notable era of discovery. There is a promising future for preventing and treating this common and troubling condition that affects not just the mouth but also the whole body.

Host modulation for the treatment of periodontal disease.

Until the 1970s, treatment strategies for periodontal diseases were primarily based on the understanding that plaque bacteria and their products mediated the tissue destruction in periodontal patients. This concept began to change, however, when investigators reported that host responses to the causative bacteria were a major contributor to disease pathogenesis. With a new understanding of host response and periodontal disease pathogenesis, it became apparent that inhibition of certain host response pathways might be an additional strategy, in addition to suppressing the causative bacteria, for treating periodontal diseases. The current understanding of periodontal disease etiology and pathogenesis emphasizes the role of the host in tissue destruction (Figure1).

Histologic Evaluation of Soft and Hard Tissue Healing Following Alveolar Ridge Preservation with Deproteinized Bovine Bone Mineral Covered with Xenogenic Collagen Matrix.

The purpose of this study was to histologically evaluate new bone formation and dimensional soft tissue changes of two different healing protocols (16 weeks and 32 weeks) using deproteinized bovine bone mineral (DBBM) covered with collagen matrix (CM) for alveolar ridge preservation in the anterior esthetic zone prior to dental implant placement. Compared to baseline, both treatments yielded statistically significant differences in several clinical parameters and in the microarchitecture of the native bone and in the newly formed bone in the augmented sites. However, the protocol at 32 weeks determined greater new vital bone formation and fewer dimensional tissue changes.

Risk association between scleroderma disease characteristics, periodontitis, and tooth loss.

Systemic sclerosis (SSc) is a multi-system disorder that can have significant adverse effects on the health of the mouth. The aim of this study was to investigate the associations between the disease characteristics of SSc, periodontal disease (PD), and tooth loss. Fifty-four patients affected by SSc and 55 non-diseased controls were matched for age and gender. SSc was characterized in subtypes and with the mean duration of disease and the Modified Rodnan Skin Score [mRSS]. Patients were surveyed and examined through the evaluation of the periodontal parameters and the number of teeth. A logistic regression analysis showed that patients with SSc presented a higher number of missing teeth (p = 0.001) and a significant median increased odds 2.95 (95% CI 1.26 to 6.84) of PD (defined as clinical attachment loss, CAL) compared to nondiseased controls (6.83, 95% CI 1.94 to 24.36). Moreover, the fewer values of PD was correlated with mRSS in the total SSc group and with the mean duration of disease in patients with limited SSc (p = 0.007), even after adjusting this correlation with the presence of the major organ involvement. This study showed that patients with SSc presented increased odds of PD and tooth loss compared to non-diseased controls. In SSc patients, the magnitude of PD was strongly associated with the mRSS and with the mean duration of the disease. The clinicians should be aware of the potential systemic health problems related to PD.

Inhibition of experimental gingivitis in beagle dogs with topical mercaptoalkylguanidines.

BACKGROUND: Nitric oxide is a free radical produced in host tissues by constitutive and inducible forms of the enzyme nitric oxide synthase. Nitric oxide plays physiological roles, but it is also involved in the pathophysiology of several inflammatory conditions, including arthritis, ulcerative colitis, and circulatory shock. Local increases in inducible nitric oxide synthase (iNOS) and reactive nitrogen products have also been demonstrated in humans and animals with periodontal disease. This masked, randomized, placebo-controlled preclinical investigation examined the effect of two mercaptoalkylguanidines, mercaptoethylguanidine (MEG) and guanidinoethyldisulfide (GED), which are iNOS inhibitors and reactive nitrogen scavenging compounds, on the development of experimental gingivitis in beagle dogs. METHODS: Fifteen female, 1-year-old beagles first completed a 2-week dose-escalation experiment during which a maximum tolerated dose was determined for MEG and GED gels. Thereafter, all animals were brought to optimal gingival health by mechanical scaling, followed by rigorous daily toothbrushing over a 4-week washout period. Experimental gingivitis was then induced, with cessation of plaque control and institution of a soft diet over 8 weeks. Beagles randomly received 0.3% MEG, 0.3% GED, or placebo (vehicle) gels, topically applied twice daily to premolar teeth. Gingival inflammation, bleeding tendency, and supragingival plaque were clinically measured at baseline and at 2, 3, 4, 6, and 8 weeks. Comparisons among groups and between group pairs (active versus placebo) were made using Kruskal-Wallis tests. RESULTS: From baseline to day 7, all groups expressed similar indices. Thereafter, significant and time-dependent increases in the plaque index (PI), gingival index (GI), and percentage of bleeding on probing (%BOP) were observed in placebo-treated beagles. Mean GI scores for beagles treated with GED or MEG gels remained at or below baseline levels for the entire treatment period. At weeks 2, 3, 4, and 8, GI scores were significantly lower for MEG and GED groups compared to the placebo group (P<0.05). In addition, MEG and GED gels significantly reduced gingival bleeding responses by 8 weeks (P<0.05). Although placebo-treated beagles demonstrated %BOP scores of 43% at week 8, GED- and MEG-treated beagles exhibited %BOP scores of 21% and 26%, respectively. Since no statistical difference among PI scores was noted for any of the time points, neither mercaptoalkylguanidine appeared to affect supragingival plaque levels. CONCLUSION: The data from this preclinical study indicate that mercaptoalkylguanidines, topically administered, may significantly reduce experimental gingivitis in the beagle dog.

Risk factors for endosseous dental implant failure.

Failures of endosseous dental implants are rare and tend to cluster in patients with common profiles or risk factors. Clinical trials indicate that factors related to implant devices, anatomy, occlusion,systemic health or exposures, microbial biofilm, host immuno-inflammatory responses, and genetics may increase the risk for im-plant complications or loss. In general, factors associated with the patient appear more critical in determining risk for implant failure than those associated with the implant itself. Several risk factors can be modified. For example, the patient can modify smoking and the clinician can modify implant selection, site preparation,and loading strategy. In identifying these factors and making appropriate interventions, clinicians can enhance success rates while improving oral function, esthetics, and patient well-being.

A century of progress in understanding periodontal disease.

Throughout the 20th century, investigators and clinicians sought to discover the causes and trace the natural history of periodontal disease. Noteworthy progress has been made on several fronts. It was once believed that oral hygiene and age accounted predominantly for variances in the prevalence and severity of periodontal disease; now, a number of innate, acquired, and environmental risk factors have been identified. Light has been shed on the roles in periodontal disease pathogenesis of both specific bacteria and bacterial complexes and host immunoinflammatory responses. Insight into periodontal wound healing has fostered promising approaches to promoting regeneration of damaged periodontal structures. Finally, although theories of "focal infection" as a primary cause of systemic disease have been discredited, recent studies have confirmed the existence of an intimate connection between oral and systemic health. The progress made in understanding the nature of periodontal disease has been complemented by equally noteworthy therapeutic advances. The coupling of surgical and medical approaches to treatment ushers in a new era in the management of periodontal disease.