Experimental gingivitis: reproducibility of plaque accumulation and gingival inflammation parameters in selected populations during a repeat trial

Abstract The purpose of this study was to evaluate the relationship between volatile sulphur compounds (VSC) and gingival health status, and to monitor the changes in VSC in early dental plaque-induced gingivitis. Using an experimental gingivitis model, twelve subjects between 19 and 28 years old, with a healthy gingival status, refrained from brushing and flossing one randomly selected half of the mandibular arch for two weeks. At baseline and during six subsequent appointments, gingival inflammation (GI), bleeding on probing (BOP), and sulfide levels (SUL) were measured using the Gingival Index and the Diamond Probe/Perio 2000 System. The Spearman correlation was used to compare the relationships between SUL, GI, and BOP on the brushing (B) and non-brushing (NB) sides. Data on the NB side revealed a stronger correlation than on the B side. Wilcoxon rank sum was used to evaluate the differences between mean SUL, GI, and BOP scores on the B and NB sides over time. Results indicate that SUL were the first periodontal parameter to show a significant difference between sides. SUL were significantly higher on the NB side at 4 of the 6 data collection intervals; therefore, SUL may be associated with the initiation and progression of early plaque-induced gingivitis. Citation Zhou H, McCombs GB, Darby ML, et. al. Sulphur By-Product: The Relationship between Volatile Sulphur Compounds and Dental Plaque-Induced Gingivitis. J Contemp Dent Pract 2004 May;(5)2:027-039.

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Salivary levels of MPO, MMP-8 and TIMP-1 are associated with gingival inflammation response patterns during experimental gingivitis

Cytokine ◽

10.1016/j.cyto.2018.12.002 ◽

2019 ◽

Vol 115 ◽

pp. 135-141 ◽

Cited By ~ 8

Author(s):

Gustavo G. Nascimento ◽

Vibeke Baelum ◽

Timo Sorsa ◽

Taina Tervahartiala ◽

Peter D. Skottrup ◽

...

Keyword(s):

Response Patterns ◽

Gingival Inflammation ◽

Inflammation Response ◽

Experimental Gingivitis

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Modulation of Clinical Expression of Plaque-induced Gingivitis: Effect of Incisor Crown Form

Journal of Dental Research ◽

10.1177/154405910408300914 ◽

2004 ◽

Vol 83 (9) ◽

pp. 728-731 ◽

Cited By ~ 13

Author(s):

L. Trombelli ◽

R. Farina ◽

R. Manfrini ◽

D.N. Tatakis

Keyword(s):

Length Ratio ◽

Gingival Inflammation ◽

Clinical Expression ◽

Crown Length ◽

Crown Width ◽

Experimental Gingivitis ◽

Low Responder ◽

Wide Group ◽

Bleeding Score ◽

Crown Form

Evidence indicates that incisor crown form correlates with clinical periodontal features. It was hypothesized that incisor crown form may explain subject differences in gingivitis expression. The present experimental gingivitis study aimed to assess the effect of incisor crown form on plaque accumulation and gingival inflammation, and on individual susceptibility to plaque-induced gingivitis. Eighty-five periodontally healthy subjects were evaluated. A negative correlation was found between incisor crown width/crown length ratio and bleeding score (p = 0.045). From the 85 subjects, two groups of subjects with either ‘long-narrow’ or ‘short-wide’ incisor form were identified. The ‘long-narrow’ group had a significantly higher bleeding score than the ‘short-wide’ group (p = 0.014). No significant differences were found in the incisor crown width/crown length ratio between previously identified ‘high responder’ and ‘low responder’ subjects ( Trombelli et al., 2004a ). In conclusion, incisor crown form appears to affect the bleeding response of inflamed gingival tissues, while it exerts no influence on explaining differences in individuals’ susceptibility to plaque-induced gingivitis.

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Bleeding Index and Monocyte Chemoattractant Protein 1 as Gingival Inflammation Parameters after Chemical-Mechanical Retraction Procedure

Medical Principles and Practice ◽

10.1159/000506878 ◽

2020 ◽

Vol 29 (5) ◽

pp. 492-498

Author(s):

Marko Igic ◽

Milena Kostic ◽

Jelena Basic ◽

Nebojsa Krunic ◽

Ana Pejcic ◽

...

Keyword(s):

Gingival Inflammation ◽

Monocyte Chemoattractant Protein 1 ◽

Monocyte Chemoattractant ◽

Monocyte Chemoattractant Protein ◽

Inflammation Parameters

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Acute phase reactants - A review

CODS Journal of Dentistry ◽

10.5005/cods-6-2-96 ◽

2014 ◽

Vol 6 (2) ◽

pp. 96-101 ◽

Cited By ~ 1

Author(s):

KV Vandana ◽

KL Vandana

Keyword(s):

Acute Phase ◽

Dental Plaque ◽

Acute Phase Proteins ◽

Tissue Injury ◽

Phase Changes ◽

Gingival Inflammation ◽

Acute Phase Reactants ◽

Inflammatory Agent ◽

Experimental Gingivitis ◽

Cellular And Humoral Immunity

Abstract The acute phase refers to physiological and metabolic alterations that ensue immediately after onset of infection or tissue injury. A variety of changes in the organism act in concern to neutralize the inflammatory agent and faster healing of damaged tissues. In contrast with the specificity of cellular and humoral immunity, the acute phase changes are nonspecific and occur in response to many conditions. Periodontal disease is a chronic inflammatory process that occurs in response to a predominantly Gram-negative bacterial infection originating from dental plaque. Increased levels of acute-phase proteins have been noted with gingival inflammation, including during experimental gingivitis and periodontitis, reflecting the locally stressed environment. Here, an attempt is made to discuss the importance of acute phase reactants. How to cite this article Vandana KV, Vandana KL. Acute phase reactants - A review. CODS J Dent 2014;6;96-101

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Human variation in gingival inflammation

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.2012578118 ◽

2021 ◽

Vol 118 (27) ◽

pp. e2012578118

Author(s):

Shatha Bamashmous ◽

Georgios A. Kotsakis ◽

Kristopher A. Kerns ◽

Brian G. Leroux ◽

Camille Zenobia ◽

...

Keyword(s):

Clinical Response ◽

Host Responses ◽

Gingival Tissue ◽

Human Variation ◽

Gingival Inflammation ◽

Microbial Composition ◽

Experimental Gingivitis ◽

Bacterial Accumulation ◽

Destructive Inflammation ◽

Response Group

Oral commensal bacteria actively participate with gingival tissue to maintain healthy neutrophil surveillance and normal tissue and bone turnover processes. Disruption of this homeostatic host–bacteria relationship occurs during experimental gingivitis studies where it has been clearly established that increases in the bacterial burden increase gingival inflammation. Here, we show that experimental gingivitis resulted in three unique clinical inflammatory phenotypes (high, low, and slow) and reveal that interleukin-1β, a reported major gingivitis-associated inflammatory mediator, was not associated with clinical gingival inflammation in the slow response group. In addition, significantly higher levels of Streptococcus spp. were also unique to this group. The low clinical response group was characterized by low concentrations of host mediators, despite similar bacterial accumulation and compositional characteristics as the high clinical response group. Neutrophil and bone activation modulators were down-regulated in all response groups, revealing novel tissue and bone protective responses during gingival inflammation. These alterations in chemokine and microbial composition responses during experimental gingivitis reveal a previously uncharacterized variation in the human host response to a disruption in gingival homeostasis. Understanding this human variation in gingival inflammation may facilitate the identification of periodontitis-susceptible individuals. Overall, this study underscores the variability in host responses in the human population arising from variations in host immune profiles (low responders) and microbial community maturation (slow responders) that may impact clinical outcomes in terms of destructive inflammation.

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Local and Systemic Inflammatory Responses to Experimentally Induced Gingivitis

Disease Markers ◽

10.1155/2013/948569 ◽

2013 ◽

Vol 35 ◽

pp. 543-549 ◽

Cited By ~ 10

Author(s):

Shaneen J. Leishman ◽

Gregory J. Seymour ◽

Pauline J. Ford

Keyword(s):

Plasma Levels ◽

Inflammatory Responses ◽

Individual Variability ◽

Plaque Index ◽

Gingival Inflammation ◽

Experimental Phase ◽

Experimental Gingivitis ◽

Baseline Levels ◽

Inflammatory Burden ◽

Experimentally Induced

This study profiled the local and systemic inflammatory responses to experimentally induced gingivitis. Eight females participated in a 21-day experimental gingivitis model followed by a 14-day resolution phase. Bleeding on probing and plaque index scores were assessed before, during, and after resolution of gingival inflammation, and samples of saliva, GCF, and plasma were collected. Samples were assessed for biomarkers of inflammation using the BioPlex platform and ELISA. There were no significant changes in GCF levels of cytokines during the experimental phase; however, individual variability in cytokine profiles was noted. During resolution, mean GCF levels of IL-2, IL-6, and TNF-αdecreased and were significantly lower than baseline levels (P=0.003,P=0.025, andP=0.007, resp.). Furthermore, changes in GCF levels of IL-2, IL-6, and TNF-αduring resolution correlated with changes in plaque index scores (r=0.88,P=0.004;r=0.72,P=0.042;r=0.79,P=0.019, resp.). Plasma levels of sICAM-1 increased significantly during the experimental phase (P=0.002) and remained elevated and significantly higher than baseline levels during resolution (P<0.001). These results support the concept that gingivitis adds to the systemic inflammatory burden of an individual.

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