In Vivo Crevicular Leukocyte Response to a Chemotactic Challenge: Inhibition by Experimental Diabetes

Golub, Lorne M.; Nicoll, Gregg A.; Iacono, Vincent J.; Ramamurthy, N. S.

doi:10.1128/iai.37.3.1013-1020.1982

Cited by 50 publications

(23 citation statements)

References 35 publications

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“…However, other studies of IL-8 expression in gingival tissue and in GCF did not replicate these findings (Duarte et al 2007a, Ross et al 2010, Salvi et al 2010. Studies in diabetic rats have provided evidence of compromised gingival neutrophil function in vivo and in vitro (Ramamurthy et al 1979, Golub et al 1982 and studies in diabetic mice also suggest changes in gingival neutrophil function (Gyurko et al 2006, Sima et al 2010.…”

Section: Immune Cell Functionmentioning

confidence: 99%

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

Taylor

Preshaw

Lalla

2013

J Clinic Periodontology

338

121

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Aims: To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. Methods: Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. Results: Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small-scale clinical studies and experiments in animal models suggest that IL-1b, TNF-a, IL-6, OPG and RANKL may mediate periodontitis in diabetes. The AGE-RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetesassociated periodontitis. A role for locally activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. Conclusion: There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro.

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Section: Immune Cell Functionmentioning

confidence: 99%

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

Taylor

Preshaw

Lalla

2013

J Clinic Periodontology

338

121

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“…Other studies have shown, however, that diabetes increases the in vitro collagenase activity of gingiva from germ-free rats, thus pro-viding evidence that the effeet is at least in part, endogenously mediated (70), Extraeted collagenase from human gingiva has been found to be positively related to the severity of inflammatory periodontal disease (71), and recently Ramamurthy and Golub (72) have demonstrated in vivo diabetes-induced enhanced gingival collagenase activity in streptozotocin diabetic rats, thus establishing one of the possible meehanisms for increased periodontal disease in the diabetie patient, Neutrophils play a primary role in the proteetion against baeterial infeetion and reeent research has emphasized altered polymorphonuelear leukoeyte (PMN) function as a significant factor in the relationship between diabetes and periodontal disease (73,74,75), Impairment of PMN ehemotactic response in diabetics with severe periodontitis as measured by clinical parameters has been demonstrated (73), Golub et al, (74) monitored PMN ehemotaxis in the gingival ereviee in vivo and found a marked suppression of the in vivo crevicular response to the two ehemotactic agents, ca.scin and N-formylmethionylleueylphenylalanine (FMLP). Clark (75) has classified the PMN disorder associated with diabetes as a eellular defeet, based on the finding that non-diabetie relatives of diabetie patients also exhibited impaired leukocyte ehemotaxis.…”

Section: Periodontal Findingsmentioning

confidence: 99%

Diabetes mellitus and associated oral manifestations: a review

Murrah

1985

J Oral Pathology Medicine

107

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Oral research concerning diabetes mellitus has revealed a number of clinical implications. These include, among others, the need for more intense management of the diabetic patient with periodontal disease because tissue destruction may be accelerated, the need for rapid control of oral infection in these patients in order to prevent exacerbation of the existing metabolic imbalance, and the desirability of performing a screening for diabetes mellitus on all patients exhibiting asymptomatic parotid enlargement. Despite the explosion of knowledge concerning diabetes mellitus that has occurred since the discovery of insulin, its definitive etiology continues to elude the scientific community and its treatment remains in the realm of clinical management rather than in that of prevention and cure. In the past, research on diabetes has focused on the role of insulin in seeking the fundamental etiology of diabetes and its complications. With the progression of research, it has become apparent that the initiation and progression of the disease probably involve the interplay of a multiplicity of factors. Hereditary and immunologic factors, as suggested earlier, appear to be operated on by environmental factors, subsequently altering the body's metabolic milieu with widespread primary and secondary effects. Fertile areas for future oral research in diabetes mellitus will include, therefore, genetics, immunology, enzymology, and basement membrane pathology. On the cellular and molecular levels, particularly, the oral cavity and associated structures comprise a somewhat under‐investigated area in diabetes mellitus research and, thus, hold great promise for increasing our knowledge of this complex disease.

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“…Diabetes of only 4 days duration began to suppress the in vivo response of crevicular leukocytes and gingival crevicular fluid typically observed in healthy animals. 23,24 The reduced response became more severe with longer duration of diabetes and with greater severity of the hyperglycémie state. Indeed, diabetes of 4, 10 to 14, and 20 days duration reduced the peak PMNL response 45, 66, and 71%, respectively (Fig.…”

Section: Methods and Resultsmentioning

confidence: 99%

“…In vitro chemotactic activity of PMNLs from peritoneal exudates from the three groups of rats was then determined by the agarose technique, as described previously. [20][21][22][23][24][25][26][27][28][29][30][31][32][33] In vitro chemotactic activity, calculated as the chemo- Each vertical bar represents the mean ± SEM of the baseline values or the peak values for the C and D rats independent of time. The number on lop ofeach cross-hatched bar is the mean time (minutes) required to reach the peak response.…”

Section: Methods and Resultsmentioning

confidence: 99%

“…23 We determined that this in vivo technique detected reduced PMNL migration in the gingival sulci of diabetic rats which correlated with defective chemotactic activity assayed by an in vitro technique. 24 We subsequently determined that the assay detected an atypical and reduced crevicular PMNL response pattern in patients with LJP.25 In this review, ( 1 ) the development of the in vivo assay is outlined, (2) data obtained from tests of the assay on diabetic animals and on humans with various forms of periodontal disease and insulin-dependent diabetes mellitus (IDDM) are presented and (3) potential applications of the technique are discussed.…”

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confidence: 99%

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In Vivo Assay of Crevicular Leukocyte Migration: Its Development and Potential Applications

Iacono

Singh

et al. 1985

Journal of Periodontology

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Defects in neutrophil or polymorphonuclear leukocyte (PMNL) Chemotaxis have been observed in a number of clinical conditions, including Down's syndrome and insulindependent diabetes mellitus (IDDM), which tend to be associated with severe forms of periodontal disease. In addition, impaired PMNL Chemotaxis is frequently detected in individuals with localized juvenile periodontitis (LJP). The ability to monitor PMNL function in vivo at the gingival sulcus should therefore be useful as a diagnostic test. In this regard, we developed a technique which measures the response of PMNLs to a chemotactic agent, e.g., casein and N‐formylmethionylleucylphenylalanine (N‐FMLP) placed directly into gingival crevices. The development of the technique and its relationship to in vitro assays of Chemotaxis are discussed, and data obtained from tests of the assay on control and streptozotocin‐induced diabetic rats and human subjects with various periodontal diseases and IDDM are presented. As compared with healthy subjects and control animals, atypical (double peak) and reduced crevicular PMNL response patterns were observed during oral and systemic diseases. This suggests that the in vivo assay with appropriate modifications can be used diagnostically to assess PMNL migratory dysfunction and to identify individuals who may be susceptible to severe forms of periodontal disease.

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In Vivo Crevicular Leukocyte Response to a Chemotactic Challenge: Inhibition by Experimental Diabetes

Cited by 50 publications

References 35 publications

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

Diabetes mellitus and associated oral manifestations: a review

In Vivo Assay of Crevicular Leukocyte Migration: Its Development and Potential Applications

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