Periodontal disease: associations with diabetes, glycemic control and complications

Oral Diseases (2008) 14, 191–203. doi:10.1111/j.1601-0825.2008.01442.xÓ 2008 The Authors. Journal compilation Ó 2008 Blackwell MunksgaardAll rights reserved Periodontal disease: associations with diabetes, glycemiccontrol and complications 1School of Dentistry and 2School of Public Health, University of Michigan, Ann Arbor, MI, USA OBJECTIVE: This report reviews the evidence for ad- verse effects of diabetes on periodontal health and peri- Diabetes mellitus and periodontal disease are two odontal disease on glycemic control and complications of common chronic diseases that have long been consid- ered to be biologically linked. Diabetes is an important DESIGN: MEDLINE search of the English language litera- chronic disease globally as reflected in the World ture identified primary research reports published on (a) Health Organization (WHO) declaring the rate of relationships between diabetes and periodontal diseases increase in diabetes prevalence is an epidemic. The since 2000 and (b) effects of periodontal infection on gly- WHO estimated there were 30 million people who had cemic control and diabetes complications since 1960.
diabetes worldwide in 1985. This number increased to RESULTS: Observational studies provided consistent 135 million by 1995, and reached 217 million in 2005.
evidence of greater prevalence, severity, extent, or pro- By 2030 WHO predicts this number to increase to at gression of at least one manifestation of periodontal least 366 million (Smyth and Heron, 2006). This disease in 13/17 reports reviewed. Treatment and longi- growth in diabetes prevalence, driven principally by tudinal observational studies provided evidence to sup- increasing prevalence of type 2 diabetes, is occurring in port periodontal infection having an adverse effect on both developing and developed countries. The two glycemic control, although not all investigations reported countries with the largest predicted increases are India an improvement in glycemic control after periodontal and China and the US ranked third (Smyth and Heron, treatment. Additionally, evidence from three observa- tional studies supported periodontal disease increasing Susceptible individuals with diabetes and those with the risk for diabetes complications and no published chronically poor metabolic control can experience microvascular and macrovascular complications leading CONCLUSION: The evidence reviewed supports diabe- to a significant burden for the individual and society.
tes having an adverse effect on periodontal health and This burden includes direct costs of medical care and periodontal infection having an adverse effect on glyce- indirect costs, such as lost productivity, which result mic control and incidence of diabetes complications.
from diabetes-related morbidity and premature mortal- Further rigorous study is necessary to establish unequiv- ity (Harris, 1995; Hogan et al, 2003). Health care ocally that treating periodontal infections can contribute spending for people with diabetes is more than double to glycemic control management and to the reduction of what spending would be without diabetes, and direct the burden of diabetes complications.
and indirect expenditures attributable to diabetes in 2002 in the US were conservatively estimated at $132billion, with slightly more spent on chronic complica- Keywords: periodontal disease; diabetes; epidemiology; peri- tions attributable to diabetes than on diabetes care itself (Hogan et al, 2003). The International Diabetes Feder-ation estimated that diabetes accounts for 5–10% of thetotal healthcare budget in many countries (Smyth and Correspondence: George W Taylor, School of Dentistry and School of Public Health, University of Michigan, 1011 N. University, Ann Gingivitis and periodontitis are the most common Arbor, MI 48109, USA. Tel: 734 764 1737, Fax: 734 936 1597, E-mail: periodontal diseases. For example, in the US approxi- mately 50% of the population in all age groups exhibit There are no financial relationships that may pose a conflict of reversible gingival inflammation (Albandar and King- man, 1999). Moderate or severe periodontitis, with Received 29 June 2007; revised 13 December 2007; accepted 15December 2007 destruction of periodontal attachment tissues is much less common than gingivitis yet still a common chronic been proposed to result in pertubation of cellular disease, affecting approximately 5–15% of any popula- properties, exaggerated and sustained inflammatory tion (Albandar et al, 1999; Burt, 2005).
response, impaired wound healing, and more severe Current evidence regarding the biologic link between diabetes-associated periodontal disease (Lalla et al, diabetes and periodontal disease supports diabetes and persisting hyperglycemia leading to an exaggerated The specific ways in which diabetes-enhanced inflam- immuno-inflammatory response to the periodontal mation and apoptosis may specifically impact on peri- odontal tissues of was recently thoroughly reviewed 2006; Nishimura et al, 2007), resulting in more rapid (Graves et al, 2006). In their review, Graves and and severe periodontal tissue destruction. In the meta- colleagues describe that diabetes has been reported to bolic dysregulation of diabetes, persisting hyperglycemia adversely affect bone repair by decreasing expression of causes non-enzymatic glycation and oxidation of pro- genes that induce osteoblast differentiation, and dimin- teins and lipids, and the subsequent formation of ishing growth factor and extracellular matrix production advanced glycation endproducts (AGEs), which accu- (Bouillon, 1991; Kawaguchi et al, 1994; Lu et al, 2003).
mulate in the plasma and tissues (Brownlee, 1994; One proposed mechanism for these adverse effects is Schmidt et al, 1996b; Ramasamy et al, 2005). Hyper- through the contribution of AGEs to decreased extra- glycemia and resultant AGE formation are considered cellular matrix production and inhibition of osteoblast to be a major causal factor in the pathogenesis of differentiation (McCarthy et al, 2001; Cortizo et al, 2003; Santana et al, 2003). AGEs may also delay 1994). In subjects with diabetes who also have peri- wound-healing by inducing apoptosis of extracellular- odontitis, AGEs with accompanying markers for matrix-producing cells. This enhanced apoptosis would increased oxidant stress have been demonstrated in reduce the number of osteoblastic and fibroblastic cells human gingiva (Schmidt et al, 1996a). Cell surface available for the repair of resorbed alveolar bone binding sites or receptors for AGE (RAGE) have been (Graves et al, 2006). In addition to promoting apopto- identified on the cell surfaces of several cell types sis, AGEs could affect oral tissue healing by reducing exhibiting a heightened inflammatory response and expression of collagen and promoting inflammation.
involved with the pathogenesis of complications of The mechanisms suggested for AGE-enhanced apopto- diabetes. These cell types include mononuclear phago- sis include the direct activation of caspase activity, and cytes, endothelial cells, fibroblasts, smooth muscle cells, indirect pathways that increase oxidative stress or the lymphocytes, podocytes, and neurons (Brett et al, 1993; expression of pro-apoptotic genes that regulate apopto- Ramasamy et al, 2005). The receptor for AGEs, RAGE, is the principal signal transducer for the AGE ligand(Schmidt et al, 2000).
The underlying postulate associated with these find- ings is that enhanced oxidant stress in the gingivaltissues could contribute to more frequent and more Evidence establishing the link between diabetes mellitus severe periodontal tissue destruction in individuals with and adverse effects on periodontal health have been diabetes. For example, it has been hypothesized that the extensively reviewed (Taylor, 2001; Mealey et al, 2006).
AGE-RAGE interaction induces an oxidant stress that In a narrative review of the English language literature may contribute to chronic monocytic upregulation, published between 1960 and 2000 Taylor (2001) activation of NF-jB, and subsequent expression of reported that 44 of 48 observational studies provided mRNA and secretion of proinflammatory cytokines supportive evidence of diabetes adversely affecting (such as TNF-a, IL-1b, and IL-6) by monocytic periodontal health provided (37 of the 41 cross-sectional phagocytes involved in periodontal tissue inflammation and seven of the seven cohort studies).
and destruction (Baeuerle, 1991; Schreck et al, 1991; The review conducted for this current report extends Moughal et al, 1992; Collins, 1993; Schmidt et al, 1994, that 2001 review to include reports published into 2007.
1996a; Takahashi et al, 1994; Yan et al, 1994). These The search used MEDLINE as well as reviewed mediators are recognized as effectors in periodontal reference lists of relevant papers obtained from the tissue inflammation and destruction (Salvi et al, 1998).
search to identify primary research reports on investi- Blockade of RAGE has been shown to diminish gations of relationships between diabetes/diabetes con- Porphyromonas gingivalis-triggered alveolar bone loss trol and periodontal diseases/periodontal treatment.
in the periodontium and limit the enhanced inflamma- While the literature review is extensive in conducting tory response in peripheral wounds, accelerating wound the MEDLINE search, it is not exhaustive in that no closure and facilitating angiogenesis (Lalla et al, 2000; other databases were searched. This review does not Goova et al, 2001). Additionally, AGE interaction with provide a formal assessment of the quality of the endothelial cell RAGE has been shown to enhance reports. The reports identified are displayed in table- endothelial cell vascular hyperpermeability and expres- form and the corresponding description is organized sion of vascular cell adhesion molecule-1, an adherence according to the following groupings of studies: (1) The molecule capable of attracting mononuclear cells to the effects of having diabetes on periodontal diseases in vascular wall (Schmidt et al, 1995; Wautier et al, 1996; studies that include a non-diabetes comparison group Lalla et al, 1998b). Hence, AGE-RAGE interaction has (Table 1) and (2) Effect of the degree of glycemic Periodontal disease and diabetesGW Taylor and WS Borgnakke control, usually measured by level of glycosylated increasing attention with greater numbers of publica- hemoglobin, on periodontal status in studies that tions in consecutive decades, ranging from six in the included assessment of degree of glycemic control while 1960s, eight in the 1970s, and 12 in the 1980s to 20 in the evaluating periodontal status in participants with dia- 1990s. This review identified 17 reports published in the current decade starting in the year 2000. Table 1 The reports included in Table 1 were restricted to presents a summary of the evidence on the relationship studies which compared periodontal health in subjects between diabetes and periodontal disease. Studies were with and without diabetes. This subject has attracted broadly classified and ordered by type of diabetes and Table 1 Effects of diabetes on periodontal diseases in studies including a non-diabetes control group; ordered by diabetes type and subject age Duration of diabetesDiabetes severity based onpresence of complications aDM type = diabetes type: 1 = type 1 diabetes mellitus; 2 = type 2 diabetes mellitus; 1,2 = both subjects with type 1 and type 2 diabetes mellitusincluded; GDM = gestational diabetes mellitus; 9 = diabetes type not specified and not clearly ascertainable from other information in the report.
bAges: subjects’ ages presented as minimum – maximum reported for those with a. diabetes (DM) and b. controls (Control) unless otherwisespecified.
cMeasure of periodontal disease status: Measures used include Ging = gingivitis or gingival bleeding, Ppd = probing pocket depth, Lpa = loss ofperiodontal attachment, XRBL = radiographic bone loss, JPS = juvenile periodontal score, MGI = modified gingival index, PI = Russell’sPeriodontal Index, PDR = periodontal disease rate (proportion of teeth affected by periodontal disease). The number following the measurecorresponds to greater disease in those with diabetes (1) or no difference between those with diabetes and controls (0). The letters following thenumber correspond to the parameter(s) assessed in the study: e = extent, i = incidence, p = prevalence, s = severity, r = progression.
Table 2 Effect of degree of glycemic control on periodontal status, ordered by level of evidence, diabetes type, and subject age aHierarchy of evidence based on classification scheme used (U.S. Preventive Services Task Force, 1996) where: I = evidence obtained from at leastone properly randomized controlled trial; II-1 = evidence obtained from well-designed controlled trial without randomization; II-2 = evidenceobtained from well-designed cohort or case-control analytic studies, preferably from more than one center or research group; II-3 = evidenceobtained from multiple time series with or without the intervention. Dramatic results in uncontrolled experiments (such as the results of theintroduction of penicillin treatment in the 1940s) could also be regarded as this type of evidence; III = opinions of respected authorities, based onclinical experience; descriptive studies and case reports; or reports of expert committees.
bDiabetes type: 1 = type 1 diabetes mellitus; 2 = type 2 diabetes mellitus; 1,2 = both subjects with type 1 and type 2 diabetes mellitus included;GDM = gestational diabetes mellitus; 9 = diabetes type not specified and not clearly ascertainable from other information in the report;*= diabetes type not specified but ascertained by reviewers from other information in the report or from other sources, such as directcommunication with the authors.
cEffect: 1 = subjects with poorer glycemic control had poorer health than the comparison group(s); 0 = no difference in the periodontal healthstatus between subjects with poorer glycemic control and comparison group(s).
dDiabetes types are 1 and 2 for all but one subject who had drug-induced diabetes mellitus.
age of subjects (Table 1). In contrast to seven reports of study included children only (Lalla et al, 2007), and all prospective studies published prior to 2000, all of the other studies included adult subjects, although one also studies identified for this review are cross-sectional included children or adolescents (Arrieta-Blanco et al, and thus limited in their ability to provide evidence for 2003). Two of these three studies reported greater causal inferences. There was one study of type 1 diabetes prevalence, extent, or severity of periodontal disease and it reported more extensive radiographic bone loss for at least one measure or index of periodontal disease in participants with type 1 diabetes (Tervonen et al, (Arrieta-Blanco et al, 2003; Lalla et al, 2007). One report did not find significant differences in periodontal Regarding the relationship between type 2 diabetes disease between subjects with and without diabetes and periodontitis the review identified 10 reports. One report comprised 15–45+ year olds (Endean et al, 2004), Two studies report on analyses on National Health and nine (Sandberg et al, 2000; Orbak et al, 2002; Tsai and Nutrition Examination Survey III data from over et al, 2002; Zielinski et al, 2002; Lu and Yang, 2004; 4000 women with a history of gestational diabetes Campus et al, 2005; Chuang et al, 2005; Borges-Ya´n˜ez (GDM) in the US. One report included ages 15–44 et al, 2006; Mattout et al, 2006) included only adults.
(Xiong et al, 2006) the other ages 20–59 (Novak et al, Seven of these 10 studies reported significantly poorer 2006). Both reports concluded there is a strong rela- periodontal health in subjects with type 2 diabetes, tionship between GDM and periodontal disease. Xiong whereas no significant difference was discerned in a study et al (2006) found periodontitis in 45% of pregnant of mostly older Taiwanese dialysis patients with and women with GDM vs 13% in the group without without Ôinsulin-dependent (type II) diabetes’ (Chuang diabetes, with an adjusted odds ratio of 9.11. In non- et al, 2005) as well as in a study of U. S. university clinic pregnant women, 40% of women with type 1 or 2 patients 60+ years of age with good medical and dental diabetes, 25% of those with a history of GDM, and care comparing well-controlled (mean HbA1c = 7.3% 14% of women without diabetes had periodontal with 70% having HbA1c > 7.5%) subjects with diabe- disease. The odds ratio for those with type 1 and 2 tes to subjects without diabetes (Zielinski et al, 2002); diabetes was 2.76 (Xiong et al, 2006). Novak et al (2006) whereas in a study of Mexicans 60+ years of age there found the prevalence of periodontal disease to be higher in women with a history of GDM and concluded that (P = 0.09) of periodontitis in the group with diabetes women with at history of GDM may be at greater risk (61.5%) than in the group without diabetes (49.5%) for developing more severe periodontal disease. A smaller Greek study of 34–36 weeks pregnant women Several reports consist of analyses in which subjects also concluded gingival inflammation was more pre- with type 1 and type 2 diabetes were not distinguished.
valent in the women with GDM (Mittas et al, 2006), but All of the studies in this subset were cross-sectional. One also found more plaque in that group.
Periodontal disease and diabetesGW Taylor and WS Borgnakke As with other complications of diabetes, current periodontal infection adversely affecting glycemic con- evidence also supports poorer glycemic control contrib- trol in diabetes and contributing to increased risk for uting to poorer periodontal health. Primary research the pathogenesis of diabetes complications. Because of reports in the literature published since 2000 investigat- the high vascularity of the inflamed periodontium, this ing relationships between glycemic control level and inflamed tissue may serve as an endocrine-like source periodontal disease have included studies with subjects with type 1 diabetes exclusively (one study), type 2 (Offenbacher et al, 1996; Grossi and Genco, 1998).
diabetes exclusively (seven studies), or a combination of Because of the predominance of Gram-negative anaer- individuals with either type 1 or type 2 diabetes (three obic bacteria in periodontal infection, the ulcerated studies) (Table 2). Only seven of the 12 reports pub- pocket epithelium is thought to constitute a chronic lished regard the association between degree of glycemic source of systemic challenge from bacteria, bacterial control and periodontal disease specifically in type 2 products and locally produced inflammatory media- diabetes (Sandberg et al, 2000; Tsai et al, 2002; Lu and tors. TNF-a, IL6, and IL1, all mediators important in Yang, 2004; Campus et al, 2005; Chuang et al, 2005; periodontal inflammation, have been shown to have Jansson et al, 2006; Peck et al, 2006). Five of the latter important effects on glucose and lipid metabolism, found poorer glycemic control to be a significant factor particularly following an acute infectious challenge or associated with poorer periodontal health, the associa- trauma (Feingold et al, 1989; Ling et al, 1995; Grossi tion was borderline significant in one study of dialysis and Genco, 1998). TNF-a has been reported to patients (Chuang et al, 2005) and no difference was interfere with lipid metabolism and to be an insulin found in the remaining study (Sandberg et al, 2000).
antagonist (Grunfeld et al, 1990; Feingold and Grun- Among the studies providing information on differences feld, 1992). IL6 and IL1 have also been reported to in periodontal health classified by glycemic control antagonize insulin action (Ling et al, 1995; Michie, status, most have been cross-sectional, with eight of 12 publications reporting more prevalent or more severe More direct, empirical evidence regarding the effects of periodontal disease in those with poorer glycemic periodontal infection on glycemic control of diabetes control (Tervonen et al, 2000; Tsai et al, 2002; Guzman comes from treatment studies using non-surgical peri- et al, 2003; Lu and Yang, 2004; Negishi et al, 2004; odontal therapy and observational studies (Table 3). The Campus et al, 2005; Jansson et al, 2006; Peck et al, treatment studies are a heterogeneous set of reports that 2006) and four reporting no differences (Sandberg et al, include randomized clinical trials (RCTs) and non- RCTs. The RCTs used control groups that were either Murtomaa, 2003; Chuang et al, 2005). There was one non-treated controls (Aldridge et al, 1995; Kiran et al, follow-up study identified (evidence level II-2) that was 2005), positive controls (Grossi et al, 1997; Rodrigues published since 2000 (Karikoski and Murtomaa, 2003).
et al, 2003; Skaleric et al, 2004), or controls advised to The preponderance of studies included in this review continue with their usual source of dental care (Jones of reports published since 2000 on the adverse effects of et al, 2007). Of the seven RCTs, four reported a beneficial diabetes on periodontal health are cross-sectional and effect for periodontal therapy (Grossi et al, 1997; Rodri- describe findings of convenience samples, principally gues et al, 2003; Skaleric et al, 2004; Kiran et al, 2005).
from outpatients in hospitals and clinics. While limita- An important source of variation in the RCTs is the tions on causal inference must be considered, these use of adjunctive antibiotics with the non-surgical reports continue to support previous consistent evidence periodontal therapy. Among the RCTs, four included of greater prevalence, severity or extent of at least one adjunctive antibiotics used systemically (Grossi et al, manifestation of periodontal disease in the large major- 1997; Rodrigues et al, 2003; Jones et al, 2007) or ity of studies. The reports reviewed also provide delivered locally (Skaleric et al, 2004). Three of these additional evidence to support a Ôdose-response’ rela- four RCTs using antibiotics showed beneficial effects on tionship, i.e., as glycemic control worsens, the adverse glycemic control (Grossi et al, 1997; Rodrigues et al, effects of diabetes on periodontal health become greater.
2003; Skaleric et al, 2004). However, it is important to Further, focused study of the relationship between note the significant improvement for one study was in gestational diabetes and periodontal health is emerging the positive control group that did not receive the systemic antibiotic (Rodrigues et al, 2003) and one of Finally, the findings and conclusions from this review the four RCTs reporting a beneficial effect did not use are consistent with two published meta-analyses that antibiotics (Kiran et al, 2005). Hence, to date there is no have provided quantitative summaries of the adverse clear-cut evidence to support a requirement for the use effects of diabetes on periodontal health (Papapanou, of antibiotics in combination with non-surgical peri- odontal treatment in order to observe an improvementin glycemic control associated with periodontal therapy.
Among the set of thirteen periodontal treatment Periodontal disease: its effects on glycemic studies that were not RCTs, eight reported a beneficial control and complications of diabetes mellitus effect on glycemic control (Williams and Mahan, In addition to the substantial evidence demonstrating 1960; Wolf, 1977; Miller et al, 1992; Seppala et al, diabetes as a risk factor for poor periodontal health, 1993; Seppala and Ainamo, 1994; Iwamoto et al, 2001; there is a growing body of evidence supporting Faria-Almeida et al, 2006; Schara et al, 2006) and five Periodontal disease and diabetesGW Taylor and WS Borgnakke Periodontal disease and diabetesGW Taylor and WS Borgnakke did not (Smith et al, 1996; Westfelt et al, 1996; Christ- likely to have prevalent proteinuria, and cardiovascu- gau et al, 1998; Promsudthi et al, 2005; Talbert et al, lar complications including stroke, transient ischemic 2006). Only two of these studies had control or attacks, angina, myocardial infarction, and intermit- comparison groups (Stewart et al, 2001; Promsudthi tent claudication than controls at their follow-up et al, 2005). Like the RCTs there was marked variation in the use of adjunctive antibiotics, with three of the five Two recent reports from the on-going longitudinal studies that used systemic antibiotics reporting a ben- study of diabetes and its complications in the Gila River eficial effect on glycemic control (Williams and Mahan, Indian Community in Arizona, USA, conducted by the 1960; Miller et al, 1992; Iwamoto et al, 2001).
National Institute of Diabetes and Digestive and Kidney As shown in Table 3, there is marked heterogeneity in Diseases, address nephropathy and cardiovascular dis- the studies’ designs, conduct, length of follow-up, types ease. Saremi et al (2005) studied a cohort of 628 of participants, and periodontal treatment protocols.
individuals for a median follow-up time of 11 years.
The details of the variation in this body of literature Individuals with severe periodontal disease had 3.2 times have been extensively described in several detailed greater risk for cardio-renal mortality (i.e., ischemic reviews (Grossi and Genco, 1998; Taylor, 1999; Janket heart disease and diabetic nephropathy combined) than those with no, mild, or moderate periodontal disease.
Additional evidence to support the effect of severe This estimate of significantly greater risk persisted while periodontitis on increased risk for poorer glycemic controlling for several major risk factors of cardio-renal control comes from two longitudinal observational mortality including: age, sex, diabetes duration, HbA1c, studies. A longitudinal epidemiological study of the body mass index (BMI), hypertension, blood glucose, Pima Indians in Arizona, USA (Taylor et al, 1996) cholesterol, electrocardiographic abnormalities, macro- found subjects with type 2 diabetes in good to moderate control and with severe periodontitis at baseline were In the second report Shultis et al (2007) investigated approximately six times more likely to have poor the effect of periodontitis on risk for development overt glycemic control at approximately 2-years follow-up nephropathy (macroalbuminuria) and end-stage renal than those without severe periodontitis at baseline. In disease (ESRD) in a group of 529 Gila River Indian another observational study of 25 adults with type 2 Community adults with type 2 diabetes. Their propor- diabetes, aged 58–77 years, Collin et al (1998) also tional hazards models analyses, adjusted for age, sex, reported an association between advanced periodontal diabetes duration, body mass index, and smoking, disease and impaired metabolic control.
indicated periodontitis and edentulism were significantly It is well recognized that poor glycemic control is a associated with the risk of overt nephropathy and major determinant for the development of the chronic ESRD. The incidence of macroalbuminura was 2.0, 2.1, complications of diabetes. Results from the landmark and 2.6 times greater in individuals with moderate or Diabetes Control and Complications Trial (type 1 severe periodontitis or in those who were edentulous, diabetes) and the UK Prospective Diabetes Study respectively, than those with none/mild periodontitis.
(type 2 diabetes) demonstrated that attaining and The incidence of ESRD was also 2.3, 3.5, and 4.9 times maintaining good glycemic control could reduce the greater for individuals with moderate or severe perio- risk for and slow the progression of microvascular dontitis or for those who were edentulous, respectively, complications in patients with type 1 and type 2 than those with none/mild periodontitis.
diabetes (Anonymous, 1993, 1998a,b) (Diabetes Con- The clinical and epidemiological evidence reviewed trol and Complications Trial Research Group, 1993).
provides support for the concept that periodontal Additionally, the UKPDS observed a 16% reduction infection contributes to poorer glycemic control and (P = 0.052) in the risk of combined fatal or nonfatal the risk for diabetes complications in people with myocardial infarction and sudden death. Further diabetes mellitus. However, further rigorous, controlled epidemiological analysis from the UKPDS showed a trials in diverse populations are warranted to firmly continuous association between the risk of cardio- establish that treating periodontal infections can be vascular complications and glycemia; every percentage influential in contributing to glycemic control manage- point decrease in HbAlc (e.g., 9–8%), was associated ment and possibly to the reduction of the burden of with 25% reduction in diabetes-related deaths, 7% reduction in all-cause mortality, and 18% reduction incombined fatal and nonfatal myocardial infarction There is emerging evidence from observational The evidence reviewed in this report supports previous studies regarding the association between periodontal conclusions that diabetes is associated with increased occurrence and progression of periodontitis and peri- Thorstensson et al (1996) studied 39 case-control pairs odontal infection is associated with poorer glycemic of individuals with type 1 and type 2 diabetes for control in people with diabetes. There is also evidence 6 years median follow-up time in Jo¨nko¨ping, Sweden.
emerging that gestational diabetes may adversely affect In each pair the cases had severe alveolar bone loss periodontal health. Additionally, evidence is emerging and controls had gingivitis or minor alveolar bone to suggest that periodontal disease is associated with loss. They found that cases were significantly more increased risk for diabetes complications. While treating Periodontal disease and diabetesGW Taylor and WS Borgnakke periodontal infection in people with diabetes is clearly Borges-Ya´n˜ez SA, Irigoyen-Camacho ME, Maupome G an important component in maintaining oral health, it (2006). Risk factors and prevalence of periodontitis in may also have an important role in establishing and community-dwelling elders in Mexico. J Clin Periodontol 33: maintaining glycemic control and possibly in delaying the onset or progression of diabetes complications.
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