Italiano Farmacia on line: comprare cialis senza ricetta, acquistare viagra internet.

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.
Bouillon R (1991). Diabetic bone disease. Calcif Tissue Int 49: Further rigorous, systematic study in diverse popula- Brett J, Schmidt AM, Yan SD et al (1993). Survey of the tions is warranted to support existing evidence that distribution of a newly characterized receptor for advanced treating periodontal infections can be influential in glycation end products in tissues. Am J Pathol 143: 1699– contributing to glycemic control management and possibly to the reduction of the burden of complications Brownlee M (1994). Lilly Lecture 1993. Glycation and diabetic complications. Diabetes 43: 836–841.
Burt BA (2005). Position paper: epidemiology of periodontal diseases. J Periodontol 76: 1406–1419.
Campus G, Salem A, Uzzau S, Baldoni E, Tonolo G (2005).
Diabetes and periodontal disease: a case-control study.
Drs. Taylor and Borgnakke both searched the literature for reports for possible inclusion in this manuscript.
Christgau M, Palitzsch KD, Schmalz G, Kreiner U, Frenzel S Both authors reviewed reports, conferred on which (1998). Healing response to non-surgical periodontal articles to include, and completed article assessment therapy in patients with diabetes mellitus: clinical, micro- forms, designed by Dr. Taylor, to summarize the biological, and immunologic results. J Clin Periodontol 25: content of relevance to this literature review for each included report. Dr. Taylor designed the format for the Chuang SF, Sung JM, Kuo SC, Huang JJ, Lee SY (2005). Oral tables and both authors contributed contents in the and dental manifestations in diabetic and nondiabetic tables. Both authors drafted sections of the manuscript uremic patients receiving hemodialysis. Oral Surg Oral and contributed in responding to reviewers’ comments, Med Oral Pathol Oral Radiol Endod 99: 689–695.
Collin HL, Uusitupa M, Niskanen L et al (1998). Periodontal participated in final review of the proofs, and approved findings in elderly patients with non-insulin dependent diabetes mellitus. J Periodontol 69: 962–966.
Collins T (1993). Endothelial nuclear factor-kappa B and the initiation of the atherosclerotic lesion. Lab Invest 68: 499–508.
Albandar JM, Kingman A (1999). Gingival recession, gingival Cortizo AM, Lettieri MG, Barrio DA, Mercer N, Etcheverry bleeding, and dental calculus in adults 30 years of age and SB, McCarthy AD (2003). Advanced glycation end-prod- older in the United States, 1988–1994. J Periodontol 70: 30– ucts (AGEs) induce concerted changes in the osteoblastic expression of their receptor RAGE and in the activation of Albandar JM, Brunelle JA, Kingman A (1999). Destructive extracellular signal-regulated kinases (ERK). Mol Cell periodontal disease in adults 30 years of age and older in the United States, 1988–1994. J Periodontol 70: 13–29.
Endean C, Roberts-Thomson K, Wooley S (2004). Anangu Aldridge JP, Lester V, Watts TL, Collins A, Viberti G, Wilson oral health: the status of the Indigenous population of the RF (1995). Single-blind studies of the effects of improved Anangu Pitjantjatjara lands. Australian Journal of Rural periodontal health on metabolic control in type 1 diabetes mellitus. J Clin Periodontol 22: 271–275.
Faria-Almeida R, Navarro A, Bascones A (2006). Clinical and Anonymous (1993). The effect of intensive treatment of metabolic changes after conventional treatment of type 2 diabetes on the development and progression of long-term diabetic patients with chronic periodontitis. J Periodontol complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group Feingold KR, Grunfeld C (1992). Role of cytokines in [see comments]. N Engl J Med 329: 977–986.
inducing hyperlipidemia. Diabetes 41: 97–101.
Anonymous (1998a). Intensive blood-glucose control with Feingold KR, Soued M, Serio MK, Moser AH, Dinarello CA, sulphonylureas or insulin compared with conventional Grunfeld C (1989). Multiple cytokines stimulate hepatic treatment and risk of complications in patients with type 2 lipid synthesis in vivo. Endocrinology 125: 267–274.
diabetes (UKPDS 33). UK Prospective Diabetes Study Genuth S, Eastman R, Kahn R et al (2003). Implications of (UKPDS) Group.[see comment][erratum appears in Lancet the United Kingdom prospective diabetes study. Diabetes 1999 Aug 14;354(9178):602]. Lancet 352: 837–853.
Anonymous (1998b). Effect of intensive blood-glucose con- Goova MT, Li J, Kislinger T et al (2001). Blockade of receptor trol with metformin on complications in overweight for advanced glycation end-products restores effective patients with type 2 diabetes (UKPDS 34). UK Prospec- wound healing in diabetic mice [see comment]. Am J Pathol tive Diabetes Study (UKPDS) Group.[see comment][erra- tum appears in Lancet 1998 Nov 7;352(9139):1558]. Lancet Graves DT, Liu R, Alikhani M, Al-Mashat H, Trackman PC (2006). Diabetes-enhanced inflammation and apoptosis – Arrieta-Blanco JJ, Bartolome-Villar B, Jimenez-Martinez E, impact on periodontal pathology. J Dent Res 85: 15–21.
Saavedra-Vallejo P, Arrieta-Blanco FJ (2003). Dental Grossi SG, Genco RJ (1998). Periodontal disease and diabetes problems in patients with diabetes mellitus (II): gingival mellitus: a two-way relationship. Ann Periodontol 3: 51–61.
index and periodontal disease. Medicina Oral 8: 233–247.
Grossi SG, Skrepcinski FB, DeCaro T, Zambon JJ, Cummins Baeuerle PA (1991). The inducible transcription activator NF- D, Genco RJ (1996). Response to periodontal therapy in kappa B: regulation by distinct protein subunits. Biochim diabetics and smokers. Journal of Periodontology 67: 1094– Grossi SG, Skrepcinski FB, DeCaro T et al (1997). Treatment Lu HK, Yang PC (2004). Cross-sectional analysis of different of periodontal disease in diabetics reduces glycated hemo- variables of patients with non-insulin dependent diabetes globin. J Periodontol 68: 713–719.
and their periodontal status. Int J Periodontics Restorative Grunfeld C, Soued M, Adi S, Moser AH, Dinarello CA, Feingold KR (1990). Evidence for two classes of cytokines Lu H, Kraut D, Gerstenfeld LC, Graves DT (2003). Diabetes that stimulate hepatic lipogenesis: relationships among interferes with the bone formation by affecting the expres- tumor necrosis factor, interleukin-1 and interferon-alpha.
sion of transcription factors that regulate osteoblast differ- entiation. Endocrinology 144: 346–352.
Guzman S, Karima M, Wang H-Y, Van Dyke TE (2003).
Mattout C, Bourgeois D, Bouchard P (2006). Type 2 diabetes Association between interleukin-1 genotype and periodontal and periodontal indicators: epidemiology in France 2002- disease in a diabetic population. J Periodontol 74: 1183– 2003. J Periodontal Res 41: 253–258.
McCarthy AD, Etcheverry SB, Cortizo AM (2001). Effect of Harris MI (1995). Summary National Diabetes Data Group.
advanced glycation endproducts on the secretion of insulin- Diabetes in America. 2nd ed. Washington DC: Government like growth factor-I and its binding proteins: role in Printing Office, pp. 1–13. NIH Publication no. 95-1468 osteoblast development. Acta Diabetol 38: 113–122.
Mealey BL, Oates TW, American Academy of Periodontology Hogan P, Dall T, Nikolov P, American Diabetes A (2003).
(2006). Diabetes mellitus and periodontal diseases. J Perio- Economic costs of diabetes in the US in 2002. Diabetes Care Michie HR (1996). Metabolism of sepsis and multiple organ Iwamoto Y, Nishimura F, Nakagawa M et al (2001). The failure. World J Surg 20: 460–464.
effect of antimicrobial periodontal treatment on circulating Miller LS, Manwell MA, Newbold D et al (1992). The tumor necrosis factor-alpha and glycated hemoglobin level relationship between reduction in periodontal inflammation in patients with type 2 diabetes. J Periodontol 72: 774–778.
and diabetes control: a report of 9 cases. J Periodontol 63: Janket SJ, Wightman A, Baird AE, Van Dyke TE, Jones JA (2005). Does periodontal treatment improve glycemic con- Mittas E, Erevnidou K, Koumantakis E, Papavasileiou S, trol in diabetic patients? A meta-analysis of intervention Helidonis E (2006). Gingival condition of women with studies [see comment]. J Dent Res 84: 1154–1159.
gestational diabetes on a Greek island. Spec Care Dentist 26: Jansson H, Lindholm E, Lindh C, Groop L, Bratthall G (2006). Type 2 diabetes and risk for periodontal disease: a Moughal NA, Adonogianaki E, Thornhill MH, Kinane DF role for dental health awareness. J Clin Periodontol 33: 408– (1992). Endothelial cell leukocyte adhesion molecule-1 (ELAM-1) and intercellular adhesion molecule-1 (ICAM-1) Jones JA, Miller DR, Wehler CJ et al (2007). Does expression in gingival tissue during health and experimen- periodontal care improve glycemic control? The Depart- tally-induced gingivitis. J Periodontal Res 27: 623–630.
ment of Veterans Affairs Dental Diabetes Study. J Clin Negishi J, Kawanami M, Terada Y et al (2004). Effect of lifestyle on periodontal disease status in diabetic patients.
Karikoski A, Murtomaa H (2003). Periodontal treatment J Int Acad Periodontol 6: 120–124.
needs in a follow-up study among adults with diabetes in Nishimura F, Iwamoto Y, Soga Y (2007). The periodontal Finland. Acta Odontol Scand 61: 6–10.
host response with diabetes. Periodontol 2000 43: 245–253.
Kawaguchi H, Kurokawa T, Hanada K et al (1994). Stimu- Novak KF, Taylor GW, Dawson DR, Ferguson JE II, Novak lation of fracture repair by recombinant human basic MJ (2006). Periodontitis and gestational diabetes mellitus: fibroblast growth factor in normal and streptozotocin- exploring the link in NHANES III. J Public Health Dent 66: diabetic rats. Endocrinology 135: 774–781.
Khader YS, Dauod AS, El-Qaderi SS, Alkafajei A, Batayha Offenbacher S, Katz V, Fertik G et al (1996). Periodontal WQ (2006). Periodontal status of diabetics compared with infection as a possible risk factor for preterm low birth nondiabetics: a meta-analysis [see comment in: Evid Based weight. J Periodontol 67: 1103–1113.
Dent. 2006;7(2):45; PMID: 16858380]. J Diabetes Complica- Ogunbodede EO, Fatusi OA, Akintomide A, Kolawole K, Ajayi A (2005). Oral health status in a population of Kiran M, Arpak N, Unsal E, Erdoan MF (2005). The effect of Nigerian diabetics. J Contemp Dent Pract 6: 75–84.
improved periodontal health on metabolic control in type 2 Orbak R, Tezel A, Canakci V, Demir T (2002). The influence diabetes mellitus. J Clin Periodontol 32: 266–272.
of smoking and non-insulin-dependent diabetes mellitus on Lalla E, Lamster IB, Feit M, Huang L, Schmidt AM (1998a).
periodontal disease. J Int Med Res 30: 116–125.
A murine model of accelerated periodontal disease in Papapanou PN (1996). Periodontal diseases: epidemiology.
diabetes. J Periodontal Res 33: 387–399.
Lalla E, Lamster IB, Schmidt AM (1998b). Enhanced inter- Peck T, Price C, English P, Gill G (2006). Oral health in rural action of advanced glycation end products with their cellular South African type 2 diabetic patients. Trop Doct 36: 111–112.
receptor RAGE: implications for the pathogenesis of Pickup JC, Mattock MB, Chusney GD, Burt D (1997).
accelerated periodontal disease in diabetes. Ann Periodontol NIDDM as a disease of the innate immune system: association of acute-phase reactants and interleukin-6 with Lalla E, Lamster IB, Feit M et al (2000). Blockade of RAGE metabolic syndrome X. Diabetologia 40: 1286–1292.
suppresses periodontitis-associated bone loss in diabetic Promsudthi A, Pimapansri S, Deerochanawong C, Kancha- mice. J Clin Invest 105: 1117–1124.
navasita W (2005). The effect of periodontal therapy on Lalla E, Cheng B, Lal S et al (2007). Diabetes mellitus uncontrolled type 2 diabetes mellitus in older subjects. Oral promotes periodontal destruction in children. J Clin Peri- Ramasamy R, Vannucci SJ, Yan SSD, Herold K, Yan SF, Ling PR, Istfan NW, colon E, Bistrian BR (1995). Differential Schmidt AM (2005). Advanced glycation end products and effects of interleukin-1 receptor antagonist in cytokine- and RAGE: a common thread in aging, diabetes, neurodegen- endotoxin-treated rats. Am J Physiol 268: E255–E261.
eration, and inflammation. Glycobiology 15: 16R–28R.
Periodontal disease and diabetesGW Taylor and WS Borgnakke Rodrigues DC, Taba MJ, Novaes ABJ, Souza SLS, Grisi Smyth S, Heron A (2006). Diabetes and obesity: the twin MFM (2003). Effect of non-surgical periodontal therapy on glycemic control in patients with type 2 diabetes mell- Southerland JH, Taylor GW, Moss K, Beck JD, Offenbacher S itus.[erratum appears in J Periodontol. 2004 May;75(5):780].
(2006). Commonality in chronic inflammatory diseases: periodontitis, diabetes, and coronary artery disease. Perio- Salvi GE, Beck JD, Offenbacher S (1998). PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of Stewart JE, Wager KA, Friedlander AH, Zadeh HH (2001).
periodontal disease expression. Ann Periodontol 3: 40–50.
The effect of periodontal treatment on glycemic control in Sandberg GE, Sundberg HE, Fjellstrom CA, Wikblad KF patients with type 2 diabetes mellitus. J Clin Periodontol 28: (2000). Type 2 diabetes and oral health: a comparison between diabetic and non-diabetic subjects. Diabetes Res Takahashi K, Takashiba S, Nagai A et al (1994). Assessment of interleukin-6 in the pathogenesis of periodontal disease.
Santana RB, Xu L, Chase HB, Amar S, Graves DT, Trackman PC (2003). A role for advanced glycation end products in Talbert J, Elter J, Jared HL, Offenbacher S, Southerland J, diminished bone healing in type 1 diabetes. Diabetes 52: Wilder RS (2006). The effect of periodontal therapy on TNF-alpha, IL-6 and metabolic control in type 2 diabetics.
Saremi A, Nelson RG, Tulloch-Reid M et al (2005). Peri- odontal disease and mortality in type 2 diabetes. Diabetes Taylor GW (1999). Periodontal treatment and its effects on glycemic control: a review of the evidence. Oral Surg Oral Schara R, Medvescek M, Skaleric U (2006). Periodontal Med Oral Pathol Oral Radiol Endod 87: 311–316.
disease and diabetes metabolic control: a full-mouth disin- Taylor GW (2001). Bidirectional interrelationships between fection approach. J Int Acad Periodontol 8: 61–66.
diabetes and periodontal diseases: an epidemiologic per- Schmidt AM, Hasu M, Popov D et al (1994). Receptor for spective. Ann Periodontol 6: 99–112.
advanced glycation end products (AGEs) has a central role Taylor GW, Burt BA, Becker MP et al (1996). Severe in vessel wall interactions and gene activation in response to periodontitis and risk for poor glycemic control in patients circulating AGE proteins. Proc Natl Acad Sci U S A 91: with non-insulin-dependent diabetes mellitus. J Periodontol Schmidt AM, Hori O, Chen JX et al (1995). Advanced Tervonen T, Karjalainen K, Knuuttila M, Huumonen S glycation endproducts interacting with their endothelial (2000). Alveolar bone loss in type 1 diabetic subjects. J Clin receptor induce expression of vascular cell adhesion mole- cule-1 (VCAM-1) in cultured human endothelial cells and in Thorstensson H, Kuylenstierna J, Hugoson A (1996). Medical mice. A potential mechanism for the accelerated vasculo- status and complications in relation to periodontal disease pathy of diabetes. J Clin Invest 96: 1395–1403.
experience in insulin-dependent diabetics. J Clin Periodontol Schmidt AM, Weidman E, Lalla E et al (1996a). Advanced glycation endproducts (AGEs) induce oxidant stress in the Tsai C, Hayes C, Taylor GW (2002). Glycemic control of type gingiva: a potential mechanism underlying accelerated 2 diabetes and severe periodontal disease in the US adult periodontal disease associated with diabetes. J Periodontal population. Community Dent Oral Epidemiol 30: 182–192.
U.S. Preventive Services Task Force (1996). Guide to clinical Schmidt AM, Hori O, Cao R et al (1996b). RAGE: a novel preventive services, 2nd edn. Government Printing Office: cellular receptor for advanced glycation end products.
Vlassara H (1994). Recent progress on the biologic and clinical Schmidt AM, Yan SD, Yan SF, Stern DM (2000). The biology significance of advanced glycosylation end products. J Lab of the receptor for advanced glycation end products and its ligands. Biochim Biophys Acta 1498: 99–111.
Wautier JL, Zoukourian C, Chappey O et al (1996). Receptor- Schreck R, Rieber P, Baeuerle PA (1991). Reactive oxygen mediated endothelial cell dysfunction in diabetic vasculop- intermediates as apparently widely used messengers in the athy. Soluble receptor for advanced glycation end products activation of the NF-kappa B transcription factor and HIV- blocks hyperpermeability in diabetic rats. J Clin Invest 97: Seppala B, Ainamo J (1994). A site-by-site follow-up study on Westfelt E, Rylander H, Blohme G, Jonasson P, Lindhe J the effect of controlled versus poorly controlled insulin- (1996). The effect of periodontal therapy in diabetics.
dependent diabetes mellitus. J Clin Periodontol 21: 161–165.
Results after 5 years. J Clin Periodontol 23: 92–100.
Seppala B, Seppala M, Ainamo J (1993). A longitudinal study Williams RC Jr, Mahan CJ (1960). Periodontal disease and on insulin-dependent diabetes mellitus and periodontal diabetes in young adults. JAMA 172: 776–778.
disease. J Clin Periodontol 20: 161–165.
Wolf J (1977). Dental and periodontal conditions in diabetes Shultis WA, Weil EJ, Looker HC et al (2007). Effect of mellitus. A clinical and radiographic study. Proc Finn Dent periodontitis on overt nephropathy and end-stage renal disease in type 2 diabetes. Diabetes Care 30: 306–311.
Xiong X, Buekens P, Vastardis S, Pridjian G (2006). Peri- Skaleric U, Schara R, Medvescek M, Hanlon A, Doherty F, odontal disease and gestational diabetes mellitus. Am J Lessem J (2004). Periodontal treatment by Arestin and its effects on glycemic control in type 1 diabetes patients. J Int Yan SD, Schmidt AM, Anderson GM et al (1994). Enhanced cellular oxidant stress by the interaction of advanced Smith GT, Greenbaum CJ, Johnson BD, Persson GR (1996).
glycation end products with their receptors/binding pro- Short-term responses to periodontal therapy in insulin- teins. J Biol Chem 269: 9889–9897.
dependent diabetic patients [published erratum appears in Zielinski MB, Fedele D, Forman LJ, Pomerantz SC (2002).
J Periodontol 1996 Dec;67(12):1368]. J Periodontol 67: 794– Oral health in the elderly with non-insulin-dependent diabetes mellitus. Spec Care Dentist 22: 94–98.

Source: http://odonto11unab.bligoo.cl/media/users/13/681573/files/83139/j.1601-0825.2008.01442.x.pdf

Altitude in antarctica

High Altitude Awareness Table of Contents Kirk Salveson Manager Field Science Support Raytheon Technical Services Company Polar Services 7400 S Tucson Way Centennial, Colorado 80112-3938 USA 303.790.8606, ext. 32215 September 25, 2003 Welcome to the on-line Altitude in Antarctica course. This course is designed to help you gain awareness regarding our body’s reactions and

arts-dance.org

ARTS-Dance at 55th NSDC in San Antonio, TX In its efforts to fulfill the ARTS Mission the ARTSThe updated ARTS Tri-Fold brochure was inserted into theGoverning Board has identified new opportunities toregistration packets of convention attendees. There wasgenerate public awareness and promote growth andgood attendance as well as participation in the seminaracceptance of contemporary Squ

Copyright © 2010-2014 Drugstore Pdf Search