A New Era for the Oral Microbiome

Jakubovics, Nicholas S.; Shi, Wenyuan

doi:10.1177/0022034520918536

Cited by 10 publications

(10 citation statements)

References 34 publications

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“…The humoral immune system provides a critical component of the host control of infectious agents. Periodontitis represents a process in which the oral microbiome at sites of lesions transitions to dysbiosis 1,52–55 . Substantial evidence is available regarding the induction of local and systemic‐specific antibodies to oral bacteria that are altered in the dysbiotic microbiome of periodontitis and support that antibody can provide some protection against the development of periodontitis 38,56–58 .…”

Section: Discussionmentioning

confidence: 99%

Gingival tissue antibody gene utilization in aging and periodontitis

Ebersole

Linh-Trung

González

2022

J of Periodontal Research

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Objective This study used a nonhuman primate model of ligature‐induced periodontitis to document the characteristics of immunoglobulin (Ig) gene usage in gingival tissues with disease and affected by age. Background Adaptive immune responses to an array of oral bacteria are routinely detected in local gingival tissues and the systemic circulation across the human population. The level and diversity of antibody increases with periodontitis, reflecting the increased quantity of B cells and plasmacytes in the tissues at sites of periodontal lesions. Methods Macaca mulatta (n = 36) in four groups (young – ≤3 years; adolescent >3–7 years; adult – 12–15 years; aged – 17‐23 years) were used in this study. Gingival tissues were sampled at baseline (health), 2 weeks (initiation), 1 and 3 months (progression), and 5 months (resolution) of the lesion development and transcriptomic analysis included 78 Ig‐related genes. Results The results demonstrated extensive variation in Ig gene usage patterns and changes with the disease process that was substantially affected by the age of the animal. Of note was that the aged animals generally demonstrated elevated expression on multiple Ig genes even in the baseline/healthy gingival tissues. The expression levels revealed 5 aggregates of Ig gene change profiles across the age groups. The number of gene changes were greatly increased in adult animals with the initiation of disease, while the young and adolescent animals showed extensive changes with disease progression. Elevated Ig gene transcripts remained with disease resolution except in the aged animals. The response profiles demonstrated selective heavy/light change gene transcripts that differed with age and clustering of the transcript expression was dominated by the age of the animals. Conclusions The results suggested potential critical variations in the molecular aspects of Ig gene expression in gingival tissues that can contribute to understanding the kinetics of periodontal lesions, as well as the variation in episodes, rapidity of progression, and role in resolution that are impacted by age.

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Section: Discussionmentioning

confidence: 99%

Gingival tissue antibody gene utilization in aging and periodontitis

Ebersole

Linh-Trung

González

2022

J of Periodontal Research

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“…Clear evidence is available regarding the initiation and development of the complex microbiome in the oral cavity. Existing data have demonstrated unique features of the microbiome in different niches in the oral cavity [3,39,40], periodontitis vs. healthy periodontium in adults demonstrating the effect of smoking and diabetes on the microbiome [2,5,[41][42][43][44][45], progressing vs. non-progressing periodontal sites [46][47][48], and distribution of the large array of species across human populations [5,49]. Chronic periodontal infections provide a very different "face" to the host with regards to controlling these bacteria.…”

Section: Discussionmentioning

confidence: 99%

“…This disease is accentuated with age, likely reflecting a combination of general tissue health and remodeling capabilities, long-term environmental and epigenetic effects on tissue homeostasis and the oral microbiome, and immunosenescent changes in the host response profile [1]. This dysbiotic microbiome displays an altered presence and an abundance of microbial members, selected microorganisms that appear to directly facilitate changes in the local environment enhancing a more pathogenic microbiome, and altered gene expression profiles of normal commensal bacteria that can contribute to altering the host-inflammatory response [2][3][4][5]. Approaches to lessen this microbial burden through both mechanical and chemical strategies generally show a high frequency of positive responses across the population in decreasing the continuation of these lesions [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Oral Microbiome and Gingival Gene Expression of Inflammatory Biomolecules With Aging and Periodontitis

Ebersole

Nagarajan

Kirakodu

et al. 2021

Front. Oral. Health

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Although data describe the presence and increase of inflammatory mediators in the local environment in periodontitis vs. health in humans, details regarding how these responses evolve in the transition from health to disease, changes during disease progression, and features of a resolved lesion remain unknown. This study used a nonhuman primate model of ligature-induced periodontitis in young, adolescent, adult, and aged animals to document features of inflammatory response affected by age. Rhesus monkeys had ligatures tied and provided gingival tissue biopsy specimens at baseline, 0.5, 1, and 3 months of disease and at 5 months of the study, which was 2 months post-ligature removal for clinically resolved tissues. The transcriptome was assessed using microarrays for chemokine (n = 41), cytokine (n = 45), chemokine receptor (n = 21), cytokine receptor (n = 37), and lipid mediator (n = 31) genes. Limited differences were noted in healthy tissues for chemokine expression with age; however, chemokine receptor genes were decreased in young but elevated in aged samples. IL1A, IL36A, and IL36G cytokines were decreased in the younger groups, with IL36A elevated in aged animals. IL10RA/IL10RB cytokine receptors were altered with age. Striking variation in the lipid mediator genes in health was observed with nearly 60% of these genes altered with age. A specific repertoire of chemokine and chemokine receptor genes was affected by the disease process, predominated by changes during disease initiation. Cytokine/cytokine receptor genes were also elevated with disease initiation, albeit IL36B, IL36G, and IL36RN were all significantly decreased throughout disease and resolution. Significant changes were observed in similar lipid mediator genes with disease and resolution across the age groups. Examination of the microbiome links to the inflammatory genes demonstrated that specific microbes, including Fusobacterium, P. gingivalis, F. alocis, Pasteurellaceae, and Prevotella are most frequently significantly correlated. These correlations were generally positive in older animals and negative in younger specimens. Gene expression and microbiome patterns from baseline were distinctly different from disease and resolution. These results demonstrate patterns of inflammatory gene expression throughout the phases of the induction of a periodontal disease lesion. The patterns show a very different relationship to specific members of the oral microbiome in younger compared with older animals.

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“…It is still not clear which of the species or complexes of bacteria are aetiologic in the initiation and progression of a disease lesion; however, substantial information has documented their ability to elicit biologic responses from various host cells that could account for the tissue breakdown of periodontitis 11–17 . However, the current paradigm of the microbiology of periodontitis focuses on the importance of the overall microbiome, interactions including co‐operation and competition among the members, and synergism in the virulence potential of the altered, that is dysbiotic, disease microbiome 18,19 …”

Section: Introductionmentioning

confidence: 99%