Gingival Crevicular Fluid Levels of Interleukin‐1β and Glycemic Control in Patients With Chronic Periodontitis and Type 2 Diabetes

Engebretson, Steven P.; Hey-Hadavi, Judith; Ehrhardt, Fernando J.; Hsu, David; Celenti, Romi S.; Grbic, John T.; Lamster, Ira B.

doi:10.1902/jop.2004.75.9.1203

Cited by 149 publications

(142 citation statements)

References 39 publications

Supporting

Mentioning

121

Contrasting

Unclassified

Order By: Relevance

“…There is considerable evidence that diabetes enhances the innate immune response in the periodontium. IL-1beta, TNF-alpha and the chemokine MCP-1 are elevated in the gingival crevicular fluid or serum of diabetic patients and are correlated with increased periodontal tissue destruction (69)(70)(71)(72). Monocytes from patients with type 1 diabetes produce significantly greater amounts of TNF-alpha, IL-1beta and PGE2 in response to LPS compared to matched normoglycemic individuals (72,73).…”

Section: Periodontal Diseasementioning

confidence: 99%

Diabetic complications and dysregulated innate immunity

Graves

Kayal²

2008

Front Biosci

225

188

View full text Add to dashboard Cite

Diabetes mellitus is a metabolic disorder that leads to the development of a number of complications. The etiology of each diabetic complication is undoubtedly multifactorial. We will focus on one potential component that may be common in many diabetic complications, dysregulation of innate immunity associated with an increased inflammatory response. High glucose levels lead to shunting through the polyol pathway, an increase in diacylglycerol which activates protein kinase C, an increase in the release of electrons that react with oxygen molecules to form superoxides, and the non-enzymatic glycosylation of proteins that result in greater formation of advanced glycation end products. Each of these can lead to aberrant cell signalling that affects innate immunity for example, by activating the MAP kinase pathway or inducing activation of transcription factors such as NF-kappaB. This may be a common feature of several complications including periodontal disease, atherosclerosis, nephropathy, impaired healing and retinopathy. These complications are frequently associated with increased expression of inflammatory cytokines such as TNF-alpha, IL-1beta and IL-6 and enhanced generation of reactive oxygen species. Cause and effect relationship between dysregulation of key components of innate immunity and diabetic complications in many instances have been demonstrated with the use of cytokine blockers and antioxidants.

show abstract

Section: Periodontal Diseasementioning

confidence: 99%

Diabetic complications and dysregulated innate immunity

Graves

Kayal²

2008

Front Biosci

225

188

View full text Add to dashboard Cite

show abstract

“…Causes for periodontal diseases are known to be various factors, dental occurrence of periodontal disease is higher and accelerates resorption of alveolar bone, and inadequate control of blood sugar level was related to the severity of periodontal diseases [13][14][15][16][17][18][19][20][21][22][23][24][25][26] .…”

Section: Introductionmentioning

confidence: 99%

Disturbance of Periodontal Tissue Caused by Mechanical Compression into the Gingival Col of Streptozotocin-induced Diabetic Rats

Tokunaga

Enoki

Okamura

et al. 2014

J. Hard Tissue Biology.

View full text Add to dashboard Cite

FThe purpose of this study is to clarify the destructive processes of periodontal tissue, especially of alveolar bone, induced by food impaction. Streptozotocin-induced diabetic rat was used, gutter percha point (GP) was inserted into interdental gingival col space between upper M1 and M2, and the change of body weight, histopathological findings and 3D SEM structure of alveolar bone were compared between diabetic (Group DM) and control (Group N) animals (Experiment 1). Large amounts of bacterial deposits and sequester were observed at the alveolar crest, and subsequently experiment 2 was carried out to explore the relationship between bacterial infection and sequester formation. The combination of mechanical compression and daily twice cleaning with 3% oxydol and Periocline were carried out. As a result of experiment 1, ulceration with partial exposure of alveolar crest, inflammatory infiltrates and hyaline degeneration occurred in the col, and bone resorption was scarcely observed at 1d in Group N. Bone resorption of alveolar bone progressed at 3d and 5d, decreasing the height of alveolar crest and the width of alveolar bone. Reepithelization of ulcer surface was observed at 7d and 14d, and concurrently bone resorption regressed and new bone formation suggested reparative changes. SEM observation confirmed these changes of alveolar bone. On the contrary, massive bacterial deposits were observed, and bone resorption was scanty in the upper region and slight in the middle to lower region of alveolar bone at 1 day of Group DM. Massive bacterial deposits with partial exposure of alveolar bone were observed at 3d and 5d, and sequester was isolated owing to intense undermining bone resorption. Regeneration of epithelium was seen beneath the sequester at 14d, showing the phenomenon of foreign body exclusion. The light microscopic changes of Group DM were consistent with SEM findings. The total number of osteoclasts was fewer at 1d and larger at 3d and 5d in Group DM. Osteoclasts at the upper region of alveolar bone increased from 1d to 5d in Group N, although the number of osteoclasts did not show a significant change in Group DM. At the middle to lower portion of alveolar bone, the number of osteoclast was significantly fewer at 1d, larger at 3d and 5d in Group DM. In experiment 2, the col with ulceration and necrosis did not show bacterial deposits or sequester, suggesting the intimate relation between bacterial infection and sequestration. The present study suggests that food impaction and subsequent mechanical compression to the col could induce various damages of periodontal tissue, including sequester formation, and elaborate plaque control at the initial stage of food impaction could prevent sequester formation and protect the height of alveolar bone.

show abstract

“…AGE alter the immune response in T2D with up‐regulation of pro‐inflammatory cytokines, e.g., Tumor Necrosis Factor‐α (TNF‐α) (Ramasamy, Yan, & Schmidt, 2012), which in turn is believed to influence the progression of PD (Lalla & Papapanou, 2011). Furthermore, T2D affects the oral environment with higher glucose levels and pro‐inflammatory mediators in the gingival crevicular fluid, which have been regarded key mechanisms for modifying the microbiota in T2D patients (Engebretson et al, 2004; Ficara, Levin, Grower, & Kramer, 1975). Recent studies have demonstrated different bacterial profiles of subgingival plaque in T2D patients with chronic PD as compared to PD patients without T2D (Casarin et al, 2013; Zhou et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Ligature‐associated bacterial profiles are linked to type 2 diabetes mellitus in a rat model and influenced by antibody treatment against TNF‐α or RAGE

Grauballe

Belstrøm

Østergaard

et al. 2017

Clinical & Exp Dental Res

View full text Add to dashboard Cite

There is a bidirectional relationship between periodontal disease (PD) and type 2 diabetes mellitus (T2D). T2D may lead to ecological perturbations in the oral environment, which may facilitate an altered microbiota. However, previous studies have been inconclusive in determining the effect of T2D on oral bacterial profiles. Therefore, we aimed to evaluate the influence of T2D on the ligature‐associated bacterial profile in a diabetic rat model with PD and investigated the impact of blocking inflammatory pathways with antibodies targeting either Tumor Necrosis Factor α (TNF‐α) or the receptor of advanced glycation end‐products (RAGE). A total of 62 Zucker obese rats (45 T2D) and 17 lean (non‐T2D) were divided into 4 treatment groups; lean with PD, obese with PD, obese with PD and anti‐TNF‐α treatment, and obese with PD with anti‐RAGE treatment. Periodontal disease was ligature induced. Ligature‐associated bacterial profiles were analyzed using Human Oral Microbe Identification Microarray (HOMIM). Ligature‐associated bacterial profiles differed between lean and obese rats. Furthermore, treatment with antibodies against TNF‐α or RAGE had an impact on subgingival bacterial profiles. T2D phenotypes are associated with different ligature‐associated bacterial profiles and influenced by treatment with antibodies against TNF‐α or RAGE.

show abstract

Gingival Crevicular Fluid Levels of Interleukin‐1β and Glycemic Control in Patients With Chronic Periodontitis and Type 2 Diabetes

Cited by 149 publications

References 39 publications

Diabetic complications and dysregulated innate immunity

Diabetic complications and dysregulated innate immunity

Disturbance of Periodontal Tissue Caused by Mechanical Compression into the Gingival Col of Streptozotocin-induced Diabetic Rats

Ligature‐associated bacterial profiles are linked to type 2 diabetes mellitus in a rat model and influenced by antibody treatment against TNF‐α or RAGE

Contact Info

Product

Resources

About