“Diabetes and gum disease: The diabolic duo”

BackgroundDiabetes and periodontitis have long been linked in the dental literature but have never been substantiated. Periodontitis is an oral infection affecting the tooth-supporting tissues. Although the etiology for this condition is bacterial plaque, the host immune response may also mediate destruction of the periodontal tissues. Diabetes mellitus is intricately related to the development, progression and severity of periodontitis. The literature is abundant with studies depicting this association.DiscussionDiabetes mellitus (DM) is a complex disease with varying degrees of systemic and oral complications. The periodontium is also a target for diabetic damage. In recent years, a link between periodontitis and diabetes mellitus has been postulated. The present review highlights the relationship between diabetes mellitus and periodontitis. The potential mechanisms involved in the development of periodontitis in diabetic patients, influence of periodontitis on diabetes and the role of TNF-α, a prime inflammatory mediator linking both of them have been discussed.ConclusionDiabetes clearly increases the risk of periodontal diseases, and biologically plausible mechanisms have been demonstrated in abundance. Less clear is the impact of periodontal diseases on glycemic control of diabetes and the mechanisms through which this occurs. It is possible that periodontal diseases may serve as initiators or propagators of insulin resistance in a way similar to obesity, thereby aggravating glycemic control.     

Infection and periodontal diseases

Contemporary hypotheses that consider the severe forms of periodontal disease to be infections caused by site-specific microbes fail to satisfactorily explain the epidemiologic, anthropologic, and clinical features of periodontal diseases. The microbes that have been designated as periodontopathogens are commensal bacteria present in periodontal health and disease. Association of specific bacteria with various disease forms has been established, but association is confused with causation. None of the periodontal diseases can be transmitted between individuals or between diseased and healthy sites of a susceptible person. Past and present concepts of the etiology of the periodontal diseases are reviewed, and the deficiencies of contemporary periodontal theory are outlined. Host factors rather than bacteria determine whether gingivitis extends to horizontal periodontitis. Angular alveolar lesions, the severe form of periodontal bone loss, are hypothesized to be caused by the spread of pulpal inflammation to the adjacent periodontal tissues. When the resultant dental abscess becomes contiguous with the alveolar crest and gingival sulcus, secondary colonization of deep pockets by site-specific oral bacteria-selected for by the complex conditions of the site-can occur. This explanation accounts for the distribution of periodontopathogens, the localization of angular alveolar lesions, and the bursts of activity by which the disease progresses.     

Periodontal diseases and diabetes

Inflammatory periodontal diseases are common in the United States. The incidence of gingivitis and periodontitis appears to be the same for persons with controlled diabetes as for those in the nondiabetic population. For patients with uncontrolled diabetes, however, periodontal diseases progress more rapidly than in their controlled counterparts. In addition, once a person with diabetes has periodontitis, the disease is usually more aggressive than in nondiabetic controls. These differences may be due to microangiopathy, altered polymorphonuclear leukocyte chemotaxis, increased dental plaque formation, or other causes. Patients with diabetes should be counseled to have a periodontal screening, which must include the use of a probe to measure the depth of the periodontal pockets. When problems are found, they should be treated and the patient should be placed in maintenance therapy.     

Dentistry and internal medicine: from the focal infection theory to the periodontal medicine concept

During past decades the relationship between dentistry and internal medicine and especially the concept of the so-called focal infection theory have long been a matter of debate. The pathogenesis of focal diseases has been classically attributed to dental pulp pathologies and periapical infections. Nonetheless, in recent years, their role is being dismissed while increasing interest is being devoted to the possible associations between periodontal infection and systemic diseases. In fact, periodontal pathogens and their products, as well as inflammatory mediators produced in periodontal tissues, might enter the bloodstream, causing systemic effects and/or contributing to systemic diseases. On the basis of this mechanism, chronic periodontitis has been suggested as a risk factor for cardiovascular diseases associated with atherosclerosis, bacterial endocarditis, diabetes mellitus, respiratory disease, preterm delivery, rheumatoid arthritis, and, recently, osteoporosis, pancreatic cancer, metabolic syndrome, renal diseases and neurodegenerative diseases such as Alzheimer's disease. Various hypotheses, including common susceptibility, systemic inflammation, direct bacterial infection and cross-reactivity, or molecular mimicry, between bacterial antigens and self-antigens, have been postulated to explain these relationships. In this scenario, the association of periodontal disease with systemic diseases has set the stage for introducing the concept of periodontal medicine. This narrative review summarizes the evolution of focal infection theory up to the current pathophysiology of periodontal disease, and presents an update on the relationships between chronic periodontitis and systemic diseases.     

Dental and periodontal lesions in patients with gastro-oesophageal reflux disease

OBJECTIVE: Dental erosion has been considered an extraesophageal manifestation of gastro-oesophageal reflux disease, but few reports have studied the relationship between this disease and other periodontal or dental lesions. The aim of this study was to investigate the prevalence of dental and periodontal lesions in patients with gastro-oesophageal reflux disease. PATIENTS AND METHODS: A total of 253 subjects were prospectively studied between April 1998 and May 2000. Two study groups were established: 181 patients with gastro-oesophageal reflux disease and 72 healthy volunteers. Clinical assessment, including body mass index and consumption of tobacco and alcohol, was performed in all subjects, as well as a dental and periodontal examination performed by a dentist physician, blind as to the diagnosis of subjects. Parameters evaluated were: (a) presence and number of dental erosion, location and severity, according to the Eccles and Jenkins index [Prosthet Dent 1979;42:649-53], modified by Hattab [Int J Prosthes 2000;13:101-71; (b) assessment of dental condition by means of the CAO index; and (c) periodontal status analysed by the plaque index, the haemorrhage index, and gingival recessions. RESULTS: Clinical parameters were similar in both groups (p > 0.05). Age was statistically associated with the CAO index, presence of dental erosion, and gingival recession (p < 0.001, Student's t-test). Compared with the control group, the percentage of dental erosion was significantly higher in the gastro-oesophageal reflux disease group (12.5 vs. 47.5%, p < 0.001, chi2-test), as was the number and severity of dental erosions (p < 0.001, Student's t-test). Location of dental erosion was significantly different between groups. Age was not statistically related to either the amount or severity of dental erosion. CAO and periodontal indices were similarly distributed between groups. CONCLUSIONS: Dental erosion may even be considered as an extraesophageal manifestation of gastro-oesophageal reflux disease. The fact that the prevalence of caries and periodontal lesions is similar in patients with gastro-oesophageal reflux disease and in healthy volunteers suggests a lack of relationship with gastro-oesophageal reflux disease.     

Metabolic syndrome and gastrointestinal diseases

Metabolic syndrome is a cluster of metabolic abnormalities consisting essentially of obesity, especially abdominal obesity. Metabolic syndrome has been highlighted as a risk factor for cardiovascular and other chronic diseases. Obesity has been implicated in various gastrointestinal diseases such as gastroesophageal reflux diseases and colorectal cancer. Recently, abdominal obesity has been shown to be more important than obesity as expressed by an elevated body mass index as a causative factor for the development of these diseases. In addition to the mechanical effects of obesity, such as an increase in intra-abdominal pressure from large amounts of adipose tissue, substances that adipose tissues secrete, such as tumor necrosis factor-α, interleukin-6, leptin, and insulin-like growth factor-1, have been proposed to be pathogenic links to these diseases. In this review, we discuss the association of metabolic syndrome or the individual components of metabolic syndrome, focusing on obesity and abdominal obesity, with gastrointestinal diseases.     

Is subclinical cardiovascular disease linked with periodontal disease in diabetic and non-diabetic subjects?

Periodontal disease leads to a systemic hyper-inflammatory state that might impair other co-morbidities including cardiovascular disease. Evidence-based findings showed that periodontitis may be linked with subclinical signs of cardiovascular diseases such as arterial stiffness. Nevertheless, some contrasting results have been reported over the years. A cross-sectional study regarding the relationship between periodontal disease and subclinical cardiovascular diseases, in non-diabetic and diabetic individuals, has been recently published. Therefore, the aim of this commentary is to give an in-depth on this topic.     

Obesity-related cardiovascular risk in children and the role of lifestyle changes

Overweight and obesity in children present significant public health concerns because of the link with numerous chronic health conditions, especially type 2 diabetes and cardiovascular disease. Perhaps obesity is only the visible pointer of other underlying risk factors for these disease conditions in childhood. Although an imbalance between energy consumed and expended appears to be the simplistic underlying problem for the increased prevalence of obesity, it is a complex condition, with various contributing factors, and may be considered the metabolic factory for various risk factors for cardiovascular disease, both modifiable and nonmodifiable. It has also been recognized that the risk factors emerge quite early in the clinical course of obesity. Physical activity-based lifestyle change appears to be the most variable component of energy expenditure and therefore has been the obvious choice and the target of behavioral interventions to modify body weight in children. This review focuses on the obesity-related nontraditional risk factors for cardiovascular disease in children and the role of lifestyle changes in modulating these risk factors.     

Immune dysregulation mediated by the oral microbiome: potential link to chronic inflammation and atherosclerosis

Cardiovascular disease is an inflammatory disorder characterized by the progressive formation of plaque in coronary arteries, termed atherosclerosis. It is a multifactorial disease that is one of the leading causes of death worldwide. Although a number of risk factors have been associated with disease progression, the underlying inflammatory mechanisms contributing to atherosclerosis remain to be fully delineated. Within the last decade, the potential role for infection in inflammatory plaque progression has received considerable interest. Microbial pathogens associated with periodontal disease have been of particular interest due to the high levels of bacteremia that are observed after routine dental procedures and every day oral activities, such as tooth brushing. Here, we explore the potential mechanisms that may explain how periodontal pathogens either directly or indirectly elicit immune dysregulation and consequently progressive inflammation manifested as atherosclerosis. Periodontal pathogens have been shown to contribute directly to atherosclerosis by disrupting endothelial cell function, one of the earliest indicators of cardiovascular disease. Oral infection is thought to indirectly induce elevated production of inflammatory mediators in the systemic circulation. Recently, a number of studies have been conducted focusing on how disruption of the gut microbiome influences the systemic production of proinflammatory cytokines and consequently exacerbation of inflammatory diseases such as atherosclerosis. It is clear that the immune mechanisms leading to atherosclerotic plaque progression, by oral infection, are complex. Understanding the immune pathways leading to disease progression is essential for the future development of anti‐inflammatory therapies for this chronic disease.     

The buccale puzzle: The symbiotic nature of endogenous infections of the oral cavity.

The indigenous, 'normal', microflora causes the majority of localized infectious diseases of the oral cavity (eg, dental caries, alveolar abscesses, periodontal diseases and candidiasis). The same microflora also protects the host from exogenous pathogens by stimulating a vigorous immune response and provides colonization resistance. How can a microflora that supports health also cause endogenous oral disease? This paradoxical host-symbiont relationship will be discussed within the dynamic of symbiosis.Symbiosis means 'life together' - it is capable of continuous change as determined by selective pressures of the oral milieu. Mutualistic symbiosis, where both the host and the indigenous microflora benefit from the association, may shift to a parasitic symbiosis, where the host is damaged and the indigenous microflora benefit. Importantly, these are reversible relationships. This microbial dynamism, called amphibiosis, is the essential adaptive process that determines the causation of endogenous oral disease by a parasitic microflora or the maintenance of oral health by a mutualistic microflora.Complex microbial consortiums, existing as a biofilm, usually provide the interfaces that initiate and perpetuate the infectious assault on host tissue. The ecology of the various oral microhabitats is critical for the development of the appropriate selecting milieux for pathogens. The microbiota associated with dental caries progression is primarily influenced by the prevailing pH, whereas periodontal diseases and pulpal infection appear to be more dependent on redox potential. Candidiasis results from host factors that favour yeast overgrowth or bacterial suppression caused by antibiotics. Oral health or disease is an adventitious event that results from microbial adaptation to prevailing conditions; prevention of endogenous oral disease can occur only when we realize that ecology is the heart of these host-symbiont relationships.     

Development of Web-based intervention system for periodontal health: a pilot study in the workplace

BACKGROUND: It has recently been accepted that periodontal disease is a risk factor for not only tooth loss but also systemic diseases. An effective system of public intervention for periodontal health to enable continuous intervention of dental professionals has been sought. We developed a Web-based intervention system regarding periodontal health and evaluated the effects of the system in the workplace. METHODS: The system was capable of storage and display of personalized oral health records including video images pertaining to toothbrush manipulation within their own oral cavities based on instructions by dental professionals. The system enabled clients to view movement of their own skill, and repeatedly. Thirteen workers of a company were randomized to either an experimental or control group. The control group received face-to-face toothbrushing instruction at the company and follow-up via telephone. The experimental group received follow-up through our system in addition to those components employed in the control group. MAIN RESULTS: The workers in the experimental group benefited in terms of improvements of not only plaque removal but also periodontal health over 3 months. CONCLUSIONS: These results indicate that implementation of an Web-based approach for periodontal health affords the possibility of remote instruction and produces additional public benefit.     

Illicit drug use and oral health

People with drug use disorders (PWDUD) have elevated prevalence of oral diseases, in particular dental caries (tooth decay), periodontal (gum) disease and xerostomia (dry mouth). When left untreated, these oral health conditions may progress and lead to tooth ache, abscesses and tooth loss, and in turn, to poor chewing functioning and digestion, dental aesthetic problems and reduced wellbeing. Illicit drug use may, per se, cause xerostomia, which in turn increases vulnerability for dental caries. However, the other main drivers of oral diseases and their progression—poor oral hygiene, frequent sugar intake and infrequent dental visits—can mainly be ascribed to the irregular lifestyle, poor economy and mental health problems that often accompany illicit drug use. Establishment of good oral health habits is essential in the dental care for PWDUD. Dental treatment is often comprehensive and challenging; because the patients may have extensive treatment needs but also difficulties adhering to preventive measures and dental appointments. An integrated care approach for PWDUD would likely benefit both their oral and general health.     

Obesity and type-2 diabetes as inducers of premature cellular senescence and ageing

Cellular senescence is now considered as a major mechanism in the development and progression of various diseases and this may include metabolic diseases such as obesity and type-2 diabetes. The presence of obesity and diabetes is a major risk factor in the development of additional health conditions, such as cardiovascular disease, kidney disease and cancer. Since senescent cells can drive disease development, obesity and diabetes can potentially create an environment that accelerates cell senescence within other tissues of the body. This can consequently manifest as age-related biological impairments and secondary diseases. Cell senescence in cell types linked with obesity and diabetes, namely adipocytes and pancreatic beta cells will be explored, followed by a discussion on the role of obesity and diabetes in accelerating ageing through induction of premature cell senescence mediated by high glucose levels and oxidised low-density lipoproteins. Particular emphasis will be placed on accelerated cell senescence in endothelial progenitor cells, endothelial cells and vascular smooth muscle cells with relation to cardiovascular disease and proximal tubular cells with relation to kidney disease. A summary of the potential strategies for therapeutically targeting senescent cells for improving health is also presented.     

The interaction between obesity and visceral hypersensitivity

Obesity has been a worldwide problem associated with numerous chronic diseases such as cardiovascular disease, type 2 diabetes, and metabolic disorders. It may also play a role in visceral hypersensitivity, contributing to irritable bowel syndrome. (i) Adipose tissue secretes various inflammatory mediators, causing intestinal hyperpermeability and nerve endings activation. (ii) Obesity and gastrointestinal microbiota could affect each other, and microbial metabolites can increase sensitivity of the colon. (iii) Vitamin D deficiency contributes to both fat accumulation and disruption of the intestinal mucosal barrier. (iv) Brain-gut axis may be another bridge from obesity to visceral hypersensitivity.     

Influence of metabolic syndrome on upper gastrointestinal disease

A recent increase in the rate of obesity as a result of insufficient physical exercise and excess food consumption has been seen in both developed and developing countries throughout the world. Additionally, the recent increased number of obese individuals with lifestyle-related diseases associated with abnormalities in glucose metabolism, dyslipidemia, and hypertension, defined as metabolic syndrome (MS), has been problematic. Although MS has been highlighted as a risk factor for ischemic heart disease and arteriosclerotic diseases, it was also recently shown to be associated with digestive system disorders, including upper gastrointestinal diseases. Unlike high body weight and high body mass index, abdominal obesity with visceral fat accumulation is implicated in the onset of various digestive system diseases because excessive visceral fat accumulation may cause an increase in intra-abdominal pressure, inducing the release of various bioactive substances, known as adipocytokines, including tumor necrosis factor-α, interleukin-6, resistin, leptin, and adiponectin. This review article focuses on upper gastrointestinal disorders and their association with MS, including obesity, visceral fat accumulation, and the major upper gastrointestinal diseases.     

Periodontal diseases

The periodontal diseases are highly prevalent and can affect up to 90% of the worldwide population. Gingivitis, the mildest form of periodontal disease, is caused by the bacterial biofilm (dental plaque) that accumulates on teeth adjacent to the gingiva (gums). However, gingivitis does not affect the underlying supporting structures of the teeth and is reversible. Periodontitis results in loss of connective tissue and bone support and is a major cause of tooth loss in adults. In addition to pathogenic microorganisms in the biofilm, genetic and environmental factors, especially tobacco use, contribute to the cause of these diseases. Genetic, dermatological, haematological, granulomatous, immunosuppressive, and neoplastic disorders can also have periodontal manifestations. Common forms of periodontal disease have been associated with adverse pregnancy outcomes, cardiovascular disease, stroke, pulmonary disease, and diabetes, but the causal relations have not been established. Prevention and treatment are aimed at controlling the bacterial biofilm and other risk factors, arresting progressive disease, and restoring lost tooth support.     

Alveolar bone loss and periodontal status in a bariatric patient: a brief review and case report

To review the effects of obesity surgery on oral health and to present a case report of the periodontal condition of an obese woman who underwent bariatric surgery. A search of studies related to bariatric surgery and oral health was made in PubMed. For case report, BMI, salivary flow, and periodontal condition were evaluated during three different periods. The oral health problems found were dental wear, periodontal diseases, xerostomia, and dental caries. The patient who was evaluated before bariatric surgery and was followed up for 2 years, lost 40.4 kg, presented normal blood glucose levels and controlled hypertension without medication. Salivary flow remained of equal value in the first year, there was an increase in mean probing depth and there existed low bone density in these sites. Patients who have undergone bariatric surgery need to be closely monitored after surgery to prevent the development of oral complications, especially periodontal conditions.     

Implications of diabetes mellitus and periodontal disease.

The dental profession is acutely aware of oral health problems associated with diabetes mellitus and clinical manifestations indicative of occult forms of the disease. Periodontal disease is common in patients with diabetes, and its effective management in diabetic patients requires cooperation involving the patient, physician, diabetes educator, dentist, and other allied health care providers. While these patients categorically appear more prone to diseases affecting the supporting tissues of the teeth, preservation of functional dental integrity can be attained by effective control of contributing systemic and local factors. This paper will discuss periodontal disease, its relationship to diabetes, proposed mechanisms of interaction, and management of periodontal disease in the diabetic patient.     

Diabetes and periodontal diseases: interplay and links

The association between diabetes and periodontal diseases is well-established. Diabetes is a risk factor for periodontal disease, with diabetic patients exhibiting an increased prevalence, extent and severity of gingivitis and perio- dontitis compared to healthy adults. Several mechanisms involved in the pathogenesis of diabetes have also been associated with periodontal disease progression. It is recognized today that there is a bidirectional relationship between diabetes and periodontal disease, with recent research showing that periodontal disease may affect the metabolic control of diabetes in diabetic patients. In this review, we present the current knowledge of the interplay between periodontal diseases and diabetes through the evaluation of randomized control and longitudinal cohort studies published in the past 15 years. Current data support the conclusion that diabetic patients are at increased risk for periodontal diseases, and that patients with poorly controlled diabetes are at risk for severe periodontitis. This results in the destruction of oral connective tissue and generalized bone loss, leading ultimately to tooth loss. Although the effect of periodontal disease on glycemic control in type 1 diabetic patients is controversial, evidence does show a direct correlation between periodontal health and glycemic control in type 2 diabetic patients. Furthermore, several studies have demonstrated the beneficial effect of periodontal treatment on metabolic control of type 2 diabetic patients.     

Roles of adiponectin and oxidative stress in obesity-associated metabolic and cardiovascular diseases

The recent increase in populations with obesity is a worldwide social problem, and the enhanced susceptibility of obese people to metabolic and cardiovascular diseases has become a growing health threat. An understanding of the molecular basis for obesity-associated disease development is required to prevent these diseases. Many studies have revealed that the mechanism involves various bioactive molecules that are released from adipose tissues and designated as adipocytokines/adipokines. Adiponectin is an adipocytokine that exerts insulin-sensitizing effects in the liver and skeletal muscle via adenosine monophosphate-activated protein kinase and proliferator-activated receptor α activation. Additionally, adiponectin can suppress atherosclerosis development in vascular walls via various anti-inflammatory effects. In contrast, oxidative stress is a harmful factor that systemically increases during obesity and promotes the development of diabetes, atherosclerosis, and various other diseases. In obese mice, oxidative stress is enhanced in adipose tissue before diabetes development, but not in the liver, skeletal muscle, and aorta, suggesting that in obesity, adipose tissue may be a major source of reactive oxygen species (ROS). ROS suppress adiponectin production in adipocytes. Treatment of obese mice with anti-oxidative agents improves insulin resistance and restores adiponectin production. Recent studies have demonstrated that adiponectin protects against oxidative stress-induced damage in the vascular endothelium and myocardium. Thus, decreased circulating adiponectin levels and increased oxidative stress, which are closely linked to each other, should be deeply involved in obesity-associated metabolic and cardiovascular disease pathogenesis.