Cognitive dysfunction in young subjects with periodontal disease.

BACKGROUND: Periodontal disease is an inflammatory, dysbiotic condition. Studies have shown that in the elderly, periodontal disease was associated with cognitive dysfunction and Alzheimer's disease. OBJECTIVE: To investigate whether young healthy subjects with periodontal disease have lower cognition compared to those without periodontal disease. The salivary cytokines (IL-1ß, TNF-α) levels in relation to cognition were also tested. METHODS: In a monocenter, cross-sectional study, forty subjects [mean age (SD) = 34 (5) and 48% female] from western Romania were classified into periodontal disease conditions using radiographic assessment: 10 subjects had aggressive periodontitis (AGG_P), 20 chronic mild-moderate periodontitis (CR_P), and 10 no periodontitis (NL_P). Neuropsychological assessment performed by standardized neurologists and psychologist included Rey Auditory Verbal Learning Test (RAVLT), Montreal Cognitive Assessment test (MOCA), Mini-Mental State Examination (MMSE), and Prague tests. Salivary cytokines levels were determined by ELISA. RESULTS: RAVLT and MOCA delayed recall scores were lower in AGG_P group compared to NL_P and CR_P. The learning curve was also different with subjects with AGG_P showing reduced learning performance. Contrary to our hypothesis, salivary IL-1ß associated with immediate but not delayed cognitive scores. CONCLUSIONS: These results showed for the first time that subjects with AGG_P had cognitive dysfunction and IL-1ß may play a role in this process.

Periodontal disease as a possible cause for Alzheimer's disease.

Approximately 47 million people worldwide have been diagnosed with dementia, 60%-80% of whom have dementia of the Alzheimer's disease type. Unfortunately, there is no cure in sight. Defining modifiable risk factors for Alzheimer's disease may have a significant impact on its prevalence. An increasing body of evidence suggests that chronic inflammation and microbial dysbiosis are risk factors for Alzheimer's disease. Periodontal disease is a chronic inflammatory disease that develops in response to response to microbial dysbiosis. Many studies have shown an association between periodontal disease and Alzheimer's disease. The intent of this paper was to review the existing literature and determine, using the Bradford Hill criteria, whether periodontal disease is causally related to Alzheimer's disease.

Is vitamin C intake too low in dialysis patients?

Vitamin C has several well-established roles in physiology including synthesis of collagen, carnitine and epinephrine, absorption of dietary iron, and mobilization of storage iron for erythropoeisis. Loss of several of these functions explains the pathology of scurvy, where defective collagen synthesis and anemia are major symptoms. Vitamin C deficiency is very common in dialysis patients and may arise from dialytic vitamin C clearance, restricted intake of vitamin C-rich foods, and increased vitamin C catabolism in vivo from inflammation. In the dialysis population, greater vitamin C intake may be needed for optimal health. Relationships between intake, body distribution, inflammation, and dialytic losses are complex and need further study. Concern about vitamin C metabolism leading to accumulation of tissue oxalate has led to the recommendation that vitamin C intake equals, but not exceeds, the intake recommended for the general population. Vitamin C deficiency in dialysis patients may have clinical consequences; a study in Renal Research Institute clinics found an association with periodontal disease. Data also support a role for vitamin C in prevention of dialysis-related anemia. New research questions are proposed in this editorial, with a discussion of strategies to determine the optimal provision of vitamin C for CKD patients.

Risk factors for osteonecrosis of the jaws: a case-control study from the CONDOR Dental PBRN.

Case reports and cohort studies have linked bisphosphonate therapy and osteonecrosis of the jaws (ONJ), but neither causality nor specific risks for lesion development have been clearly established. We conducted a 1:3 case-control study with 3 dental practice-based research networks, using dentist questionnaires and patient interviews for collection of data on bisphosphonate therapy, demographics, co-morbidities, and dental and medical treatments. Multivariable logistic regression analyses tested associations between bisphosphonate use and other risk factors with ONJ. We enrolled 191 ONJ cases and 573 controls in 119 dental practices. Bisphosphonate use was strongly associated with ONJ (odds ratios [OR] 299.5 {95% CI 70.0-1282.7} for intravenous [IV] use and OR = 12.2 {4.3-35.0} for oral use). Risk markers included local suppuration (OR = 7.8 {1.8-34.1}), dental extraction (OR = 7.6 {2.4-24.7}), and radiation therapy (OR = 24.1 {4.9-118.4}). When cancer patients (n = 143) were excluded, bisphosphonate use (OR = 7.2 {2.1-24.7}), suppuration (OR = 11.9 {2.0-69.5}), and extractions (OR = 6.6 {1.6-26.6}) remained associated with ONJ. Higher risk of ONJ began within 2 years of bisphosphonate initiation and increased 4-fold after 2 years. Both IV and oral bisphosphonate use were strongly associated with ONJ. Duration of treatment >2 years; suppuration and dental extractions were independent risk factors for ONJ.

Periodontal disease adversely affects the survival of patients with end-stage renal disease.

Periodontal disease is associated with cardiovascular disease and is thought to accelerate systemic atherosclerosis. Here we examined the relationship between periodontitis and cardiovascular disease mortality in outpatients on hemodialysis using a retrospective analysis of 168 adult patients in New York City and North Carolina. During 18 months of follow-up, cardiovascular disease and all-cause mortality were determined from a centralized dialysis registry. One hundred patients had mild or no periodontal disease but the remaining 68 had moderate-to-severe disease defined as 2 or more teeth with at least 6 mm of inter-proximal attachment loss. At baseline, the proportion of males was significantly lower in the moderate-to-severe group. Compared with mild or no periodontal disease, moderate-to-severe disease was significantly associated with death from cardiovascular causes. Adjustment for age, gender, center and dialysis vintage, smoking status, and history of diabetes mellitus or hypertension did not diminish the strength of this association. Our findings suggest a need for larger studies to confirm this connection, along with intervention trials to determine if treating periodontitis reduces cardiovascular disease mortality in dialysis patients.

Periodontitis and the end-stage renal disease patient receiving hemodialysis maintenance therapy.

Atherosclerotic complications, including myocardial infarction and stroke, are highly prevalent and associated with increased systemic inflammation in patients who have end-stage renal disease (ESRD) and are receiving renal hemodialysis maintenance therapy. In the general population, an increasing body of evidence suggests periodontitis can contribute to systemic inflammation and may contribute to atherosclerotic complications. In addition, results of recent interventional trials suggest effective periodontal therapy may decrease systemic inflammation as well as endothelial dysfunction, an early predictor of atherosclerotic complications. Because moderate-to-severe periodontitis appears to be highly prevalent in the renal hemodialysis population, effective periodontal therapy may reduce systemic inflammation and thereby become a treatment consideration for this population. This article will acquaint dental practitioners with ESRD and the association between systemic inflammation and mortality. Also discussed are the possible contributions of destructive periodontal diseases to systemic inflammation and the dental management of patients receiving renal replacement therapies.

Postoperative hypersensitivity in class I resin-based composite restorations in general practice: interim results.

Posterior permanent teeth with carious lesions radiographically extending no further than halfway into dentin (N = 565) were restored by 38 dentists in a practice-based research network, using a resin-based composite. Preoperative and 1-, 4-, and 13-week posttreatment hypersensitivity was recorded with an 11-point visual analog scale that was completed anonymously by participants. The analyses determined whether any correlation or association existed among several variables, including degree of carious activity; cavity extent; application of antimicrobial or desensitizing agents; application of liner, dentin-bonding agent and resin-based composite employed; and composite placement method. Three results were fairly unexpected: Only 36% of lesions were ranked as caries-active, 31% of teeth had appreciable preoperative hypersensitivity, and 16% of teeth with no preoperative hypersensitivity had appreciable hypersensitivity at 1 week posttreatment. Preoperative hypersensitivity was correlated with lesion visibility on radiographs but not with dentin caries activity (ranked on opening enamel), preparation depth, or preparation volume. Accrual to the study continues, and conclusions regarding other relationships await 13-week results.

Destructive periodontal diseases, systemic inflammation, and atherosclerotic complications: the emerging role of the dental profession.

An emerging body of evidence has associated moderate to severe periodontitis with atherosclerotic complications. The contribution of periodontitis to systemic inflammation may account for this association in view of the pivotal role inflammation plays in atherosclerotic complications. Periodontal therapy has been shown to decrease systemic inflammation and to improve early atherosclerotic events; however, to date, periodontal therapy has not been shown to decrease subsequent atherosclerotic complications although aggressive treatment in at-risk populations appears warranted.

Alzheimer's disease and peripheral infections: the possible contribution from periodontal infections, model and hypothesis.

Alzheimer's disease (AD) affects approximately 4.5 million people in the U.S. and this number will increase as the population ages and the life-span increases. Therefore, of paramount importance is identifying mechanisms and factors that affect the risk of developing AD. The etiology and pathogenic mechanisms for AD have not been defined, although inflammation within the brain is thought to play a role. Consistent with this hypothesis, studies suggest that peripheral infections contribute to the inflammatory state of the central nervous system. Periodontitis is a prevalent, persistent peripheral infection associated with gram negative, anaerobic bacteria that are capable of exhibiting localized and systemic infections in the host. This review offers a hypothetical link between periodontitis and AD and will present possible mechanistic links between periodontitis related inflammation and AD. It will review the pathogenesis of periodontitis and the mechanisms by which periodontal infections may affect the onset and progression of AD. Since periodontitis is a treatable condition, it may be a readily modifiable risk factor for AD.

Endotoxin levels are associated with high-density lipoprotein, triglycerides, and troponin in patients with acute coronary syndrome and angina: possible contributions from periodontal sources.

BACKGROUND: Recent studies have reported an association between poor dental health and acute coronary syndrome (ACS). The purpose of this study was to correlate the presence of periodontitis with serum endotoxin/lipopolysaccharides (LPS), lipid profiles, troponin, and immunoglobulin G (IgG) antibody to Porphyromonas gingivalis in control patients or patients with ACS or angina at the time of hospital admission. METHODS: Blood samples from 194 subjects presenting with ACS, angina, or non-cardiac chest pain were analyzed for endotoxin/LPS (Limulus amebocyte lysate assay), lipid profile, troponin, and IgG antibody to P. gingivalis. Data were collected from hospital charts and dental records, and health questionnaire responses. RESULTS: Subjects with ACS or angina were more likely to have poor oral care, fewer remaining teeth, and increased alveolar radiographic bone loss compared to subjects with chest pain. In all subjects, endotoxin/LPS and IgG antibody to P. gingivalis tended to increase in association with increased radiographic bone loss. Endotoxin/LPS increased directly with triglyceride and troponin levels (P = 0.04 and P = 0.006, respectively) and inversely with high-density lipoprotein (HDL) levels (P = 0.002). IgG antibody to P. gingivalis levels was directly correlated with very low-density lipoprotein (P = 0.03) and triglycerides (P = 0.06) and inversely with low-density lipoprotein (P = 0.01). CONCLUSIONS: Results showed more alveolar bone loss in patients with cardiac disease than in patients without cardiac disease, but there was no difference between the groups in the serum levels of endotoxin/LPS or IgG antibody to P. gingivalis. However, there were associations between endotoxin/LPS and levels of serum triglycerides, troponin, and HDL.

Treatment of deep carious lesions by complete excavation or partial removal: a critical review.

BACKGROUND: The classical approach to treatment of deep carious lesions approaching the pulp mandates removing all infected and affected dentin. Several studies call this approach into question. TYPES OF STUDIES REVIEWED: A search of five electronic databases using selected key words to identify studies relating to partial versus complete removal of carious lesions yielded 1,059 reports, of which the authors judged 23 to be relevant. Three articles reported the results of randomized controlled trials. RESULTS: The results of three randomized controlled trials, one of which followed up patients for 10 years, provide strong evidence for the advisability of leaving behind infected dentin, the removal of which would put the pulp at risk of exposure. Several additional studies have demonstrated that cariogenic bacteria, once isolated from their source of nutrition by a restoration of sufficient integrity, either die or remain dormant and thus pose no risk to the health of the dentition. CLINICAL IMPLICATIONS: There is substantial evidence that removing all vestiges of infected dentin from lesions approaching the pulp is not required for caries management.

Reduction in bacterial contamination of toothbrushes using the Violight ultraviolet light activated toothbrush sanitizer.

PURPOSE: This two armed, self-controlled, investigator blinded, clinical study tested the efficacy of an ultraviolet (UV) light toothbrush holder (Violight) to decrease toothbrush bacterial contamination. METHODS: 25 subjects were randomly assigned to control or experimental groups and received two toothbrushes for home use on either even or odd days. The control group rinsed both toothbrushes after use in cold tap water with no mechanical manipulation. The experimental group rinsed one toothbrush in cold running water while storing the other toothbrush in the Violight toothbrush holder after use. The toothbrushes were returned after 2 weeks use in sealed plastic bags and were analyzed for the number of colony forming units (CFU) of S. mutans, S. salivarius, lactobacilli, E. coli, and other coliforms, and total bacterial counts by culture. An additional analysis of the total bacterial profile was performed using denaturing gradient gel electrophoresis (DGGE). RESULTS: The Violight toothbrush holder reduced total CFU by an average of 86% (ANCOVA, P = 0.037). In addition, a tendency was noted for a reduction in total bacterial population as detected by DGGE.

Inflammation and Alzheimer's disease: possible role of periodontal diseases.

The molecular and cellular mechanisms responsible for the etiology and pathogenesis of Alzheimer's disease (AD) have not been defined; however, inflammation within the brain is thought to play a pivotal role. Studies suggest that peripheral infection/inflammation might affect the inflammatory state of the central nervous system. Chronic periodontitis is a prevalent peripheral infection that is associated with gram-negative anaerobic bacteria and the elevation of serum inflammatory markers including C-reactive protein. Recently, chronic periodontitis has been associated with several systemic diseases including AD. In this article we review the pathogenesis of chronic periodontitis and the role of inflammation in AD. In addition, we propose several potential mechanisms through which chronic periodontitis can possibly contribute to the clinical onset and progression of AD. Because chronic periodontitis is a treatable infection, it might be a readily modifiable risk factor for AD.

Effects of periodontal cell grafts and enamel matrix proteins on the implant-connective tissue interface: a pilot study in the minipig.

We have developed an experimental model to help identify and characterize factors necessary for periodontal connective tissue attachment formation on dental implants. In this pilot study, we report the effect of autogenous periodontal cell grafts, with and without the a pplication of enamel matrix derivative (EMD), on the implant-connective tissue interface. Periodontal ligament (PDL) and gingival connective tissue (GCT) cultures were established from an adult minipig. Implants were placed in osteotomies prepared with exaggerated countersinks that served as recipient sites for autogenous cell grafts in bilateral edentulated posterior mandibular sextants. In addition, 1 side received an application of EMD before placement of the autogenous cell grafts. A bioabsorbable membrane covering the coronal portion of the implants was placed before closure. After 8 weeks, quantitative histomorphometric and qualitative light microscopic analyses revealed that the implants that received gelatin vehicle alone were surrounded by bone, whereas the implants that received GCT cell grafts were mostly surrounded by fibrous connective tissue. In contrast, implants that received PDL cells without the application of EMD demonstrated good bone contact, but strands of epithelium were observed in the implant-connective tissue interface. Implants that received PDL cells and EMD also had good bone contact but without evidence of epithelium. A cementum-like interface was not observed in any of the groups. Results of this pilot study suggest that EMD and the type of cell populations present in the implant wound-healing environment may alter the implant-connective tissue interface.

Periodontal disease's contribution to Alzheimer's disease progression in Down syndrome.

People with Down syndrome (DS) are at an increased risk for Alzheimer's disease (AD). After 60 years of age, >50% of DS subjects acquire dementia. Nevertheless, the age of onset is highly variable possibly because of both genetic and environmental factors. Genetics cannot be modified, but environmental risk factors present a potentially relevant intervention for DS persons at risk for AD. Among them, inflammation, important in AD of DS type, is potential target. Consistent with this hypothesis, chronic peripheral inflammation and infections may contribute to AD pathogenesis in DS. People with DS have an aggressive form of periodontitis characterized by rapid progression, significant bacterial and inflammatory burden, and an onset as early as 6 years of age. This review offers a hypothetical mechanistic link between periodontitis and AD in the DS population. Because periodontitis is a treatable condition, it may be a readily modifiable risk factor for AD.

Opioid, NSAID, and OTC Analgesic Medications for Dental Procedures: PEARL Network Findings.

OBJECTIVE: Dental treatment is often categorized as a moderately or severely painful experience; however, no clinical data reported by the patient and dentist currently exists to support this degree of pain. This has contributed possibly to the overprescribing of analgesics, in particular the opioid class of medications. The primary objective of the study was to document the dentists' postprocedural prescriptions and recommendations for analgesic medications and their effectiveness for a 5-day period. Medications prescribed or recommended in the patient-reported outcomes included: opioid, nonsteroidal anti-inflammatory drugs (NSAIDs), and over-the-counter (OTC) analgesics. Met hods : This study used both dentist and patient responses to evaluate the use of opioid, NSAID, and OTC recommended or prescribed analgesics following one of seven classes of dental procedures encompassing over 22 specific coded procedures thought to elicit pain. The patient-centered study included a 5-day postprocedural patient follow-up assessment of the medication's effectiveness in relieving pain. RESULTS: Baseline questionnaires were completed by 2765 (99.9%) of 2767 eligible patients, and 2381 (86%) patients responded to the Day 5 follow-up questionnaires. CONCLUSION: The data suggest NSAIDs, both OTC and prescribed dosages, may be a sufficient analgesic to treat most postoperative dental pain. Clinical judgment as to the use of an opioid should include the physiological principles related to the pharmacology of pain and inflammation and may include a central effect. ClinicalTrials.gov Identifier: NCT02929602.

Case Presentations Demonstrating Periodontal Treatment Variation: PEARL Network.

BACKGROUND: Variation in periodontal terminology can affect the diagnosis and treatment plan as assessed by practicing general dentists in the Practitioners Engaged in Applied Research and Learning (PEARL) Network. General dentists participating in the PEARL Network are highly screened, credentialed, and qualified and may not be representative of the general population of dentists. METHODS: Ten randomized case presentations ranging from periodontal health to gingivitis, to mild, moderate, and severe periodontitis were randomly presented to respondents. Descriptive comparisons were made between these diagnosis groups in terms of the treatment recommendations following diagnosis. RESULTS: PEARL practitioners assessing periodontal clinical scenarios were found to either over- or under-diagnose the case presentations, which affected treatment planning, while the remaining responses concurred with respect to the diagnosis. The predominant diagnosis was compared with that assigned by two practicing periodontists. There was variation in treatment based on the diagnosis for gingivitis and the lesser forms of periodontitis. CONCLUSION: Data suggests that a lack of clarity of periodontal terminology affects both diagnosis and treatment planning, and terminology may be improved by having diagnosis codes, which could be used to assess treatment outcomes. CLINICAL IMPLICATIONS: This article provides data to support best practice for the use of diagnosis coding and integration of dentistry with medicine using ICD-10 terminology.

Periodontal disease associates with higher brain amyloid load in normal elderly.

The accumulation of amyloid-ß (Aß) plaques is a central feature of Alzheimer's disease (AD). First reported in animal models, it remains uncertain if peripheral inflammatory and/or infectious conditions in humans can promote Aß brain accumulation. Periodontal disease, a common chronic infection, has been previously reported to be associated with AD. Thirty-eight cognitively normal, healthy, and community-residing elderly (mean age, 61 and 68% female) were examined in an Alzheimer's Disease Research Center and a University-Based Dental School. Linear regression models (adjusted for age, apolipoprotein E, and smoking) were used to test the hypothesis that periodontal disease assessed by clinical attachment loss was associated with brain Aß load using (11)C-Pittsburgh compound B (PIB) positron emission tomography imaging. After adjusting for confounders, clinical attachment loss (≥3 mm), representing a history of periodontal inflammatory/infectious burden, was associated with increased PIB uptake in Aß vulnerable brain regions (p = 0.002). We show for the first time in humans an association between periodontal disease and brain Aß load. These data are consistent with the previous animal studies showing that peripheral inflammation/infections are sufficient to produce brain Aß accumulations.