Periodontitis and diabetes mellitus co-morbidity: A molecular dialogue

Luong, Anthony; Tawfik, Andy Nassif; Islamoglu, Hicret; Gobriel, Hanaa Selim; Ali, Nada; Ansari, Pouya; Shah, Ruchita; Hung, Tiffany; Patel, Tanusha; Henson, Bradley S.; Thankam, Finosh G.; Lewis, Jill B.; Mintline, Mark; Boehm, Tobias K; Tumur, Zohra; Seleem, Dalia

doi:10.1016/j.job.2021.10.006

Cited by 38 publications

(27 citation statements)

References 114 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition, the transfer of bacteria from diabetic donors to germ-free hosts induced more bone loss than transfer of bacteria from normoglycemic animals. Studies in humans are consistent with animal studies and indicate that diabetic subjects have lower oral bacterial diversity and an increase in bacterial taxa that are associated with pathogenicity ( 166 – 168 ). Interestingly, two other systemic diseases associated with greater levels of systemic inflammation, rheumatoid arthritis (RA) and lupus erythematosus have increased susceptibility to periodontal diseases and alterations in oral bacterial taxa associated with periodontal disease ( 167 ).…”

Section: Periodontal Diseasesupporting

confidence: 67%

Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

View full text Add to dashboard Cite

Periodontitis involves the loss of connective tissue attachment and alveolar bone. Single cell RNA-seq experiments have provided new insight into how resident cells and infiltrating immune cells function in response to bacterial challenge in periodontal tissues. Periodontal disease is induced by a combined innate and adaptive immune response to bacterial dysbiosis that is initiated by resident cells including epithelial cells and fibroblasts, which recruit immune cells. Chemokines and cytokines stimulate recruitment of osteoclast precursors and osteoclastogenesis in response to TNF, IL-1β, IL-6, IL-17, RANKL and other factors. Inflammation also suppresses coupled bone formation to limit repair of osteolytic lesions. Bone lining cells, osteocytes and periodontal ligament cells play a key role in both processes. The periodontal ligament contains cells that exhibit similarities to tendon cells, osteoblast-lineage cells and mesenchymal stem cells. Bone lining cells consisting of mesenchymal stem cells, osteoprogenitors and osteoblasts are influenced by osteocytes and stimulate formation of osteoclast precursors through MCSF and RANKL, which directly induce osteoclastogenesis. Following bone resorption, factors are released from resorbed bone matrix and by osteoclasts and osteal macrophages that recruit osteoblast precursors to the resorbed bone surface. Osteoblast differentiation and coupled bone formation are regulated by multiple signaling pathways including Wnt, Notch, FGF, IGF-1, BMP, and Hedgehog pathways. Diabetes, cigarette smoking and aging enhance the pathologic processes to increase bone resorption and inhibit coupled bone formation to accelerate bone loss. Other bone pathologies such as rheumatoid arthritis, post-menopausal osteoporosis and bone unloading/disuse also affect osteoblast lineage cells and participate in formation of osteolytic lesions by promoting bone resorption and inhibiting coupled bone formation. Thus, periodontitis involves the activation of an inflammatory response that involves a large number of cells to stimulate bone resorption and limit osseous repair processes.

show abstract

Section: Periodontal Diseasesupporting

confidence: 67%

Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…Por otro lado, la hiperglucemia puede promover un microbioma periodontal en condición disbiótica, favoreciendo a los patógenos bacterianos, como las especies Fusobacteria y Porphyromonas, iniciando o agravando con ello la EP. La elevación de los receptores "Toll" incrementa la respuesta del huésped al microbioma disbiótico, produciendo un aumento del estado inflamatorio (Polak et al, 2020;Luong et al, 2021).…”

Section: Resultsunclassified

Actualización de la Relación Bidireccional de la Diabetes Mellitus y la Enfermedad Periodontal

Salazar-Villavicencio

Chávez-Castillo

Carranza-Samanez

2022

Int. J. Odontostomat.

View full text Add to dashboard Cite

“…Insulin resistance and the inflammatory response are the two most important factors in the interaction between the two diseases (7). Periodontitis may aggravate diabetes as the recruited inflammatory cells and cytokines can enter into the systemic circulation to induce adipose insulin resistance (8); however, with periodontal therapy, diabetes can be effectively controlled with a decreased expression of serum TNF-a and C-reactive protein (CRP) by controlling local reactive oxygen species (ROS) levels and pro-inflammatory cytokine secretions (9), suggesting that glycemic control and anti-inflammatory therapy are equally important for tissue remodeling in diabetic periodontitis patients (10).…”

Section: Introductionmentioning

confidence: 99%

Peroxisome proliferator-activated receptor gamma preserves intracellular homeostasis of insulin-resistant periodontal ligament stem cells

et al. 2022

View full text Add to dashboard Cite

Background: Diabetes and periodontitis develop and influence each other. The peroxisome proliferatoractivated receptor gamma (PPARγ) agonist rosiglitazone (RSG) controls blood glucose and hence the systemic diseases associated with diabetes by increasing the sensitivity of tissues to insulin. However, whether and how RSG can treat diabetic periodontitis is poorly understood.Methods: Insulin-resistant periodontal ligament stem cells (IR-PDLSCs) were induced by glucosamine (18 mM, 24 h) in the presence or absence of RSG or GW9662 (a PPARγ antagonist). The glucose uptake rate was tested to evaluate insulin sensitivity. A scratch test was carried out to measure cell proliferation and motility. We used 2,7-dichlorodihydrofluorescein diacetate (DFCH-DA) and JC-1 kits to detect oxidative stress (OS), and cytoskeleton staining and Calcein-AM/PI kits were used to determine cell viability.Interferon-gamma (IFN-γ) and interleukin-10 (IL-10) ELISA kits were used to evaluate inflammation levels. Finally, quantitative real-time polymerase chain reaction (qRT-PCR) and western blot (WB) analysis were used to assess the expression of osteogenic/odontogenic differentiation-related genes or proteins.Results: Our results showed that RSG exhibited a protective effect on IR-PDLSCs, with increased insulin sensitivity and migration efficiency, an alleviation of glucosamine-induced OS, and a downregulated proinflammatory cytokine secretion through activation of PPARγ receptors. Moreover, RSG alleviated the suppressed odontogenic differentiation ability of IR-PDLSCs.Conclusions: RSG preserves the biological functions of IR-PDLSCs in maintaining intracellular homeostasis by increasing insulin sensitivity, reducing OS, and suppressing inflammation.

show abstract

Periodontitis and diabetes mellitus co-morbidity: A molecular dialogue

Cited by 38 publications

References 114 publications

Impact of the host response and osteoblast lineage cells on periodontal disease

Impact of the host response and osteoblast lineage cells on periodontal disease

Actualización de la Relación Bidireccional de la Diabetes Mellitus y la Enfermedad Periodontal

Peroxisome proliferator-activated receptor gamma preserves intracellular homeostasis of insulin-resistant periodontal ligament stem cells

Contact Info

Product

Resources

About