Oral biofilm challenge regulates the RANKL-OPG system in periodontal ligament and dental pulp cells

Belibasakis, Georgios N.; Meier, André; Guggenheim, B; Bostancı, Nagihan

doi:10.1016/j.micpath.2010.11.002

Cited by 39 publications

(41 citation statements)

References 35 publications

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“…In particular, the differential effects of these two biofilm supernatant variants were investigated on the expression of the RANKL-OPG system in GF. The findings demonstrate that both biofilm supernatants can regulate RANKL and OPG gene expressions in GF, in line with a recent study demonstrating that viable supragingival biofilms can regulate this system in periodontal ligament and dental pulp cells [19]. However, there are considerable quantitative differences in their regulatory capacity.…”

Section: Discussionsupporting

confidence: 88%

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

et al. 2011

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Periodontitis is an inflammatory condition that destroys the tooth supporting tissues, including the alveolar bone. It is triggered by polymicrobial biofilms attaching on tooth surfaces, which can be supragingival or subgingival. Bone resorption is triggered by receptor activator of NF-B ligand (RANKL) and blocked by its soluble decoy receptor osteoprotegerin (OPG), which are cytokines of the tumor necrosis factor ligand and receptor families, respectively. The present study aimed to comparatively investigate the effects of the Zürich in vitro supragingival and subgingival biofilm models, on RANKL and OPG gene expression in primary human gingival fibroblasts (GF) cultures. The cells were challenged with biofilm culture supernatants for up-to 24h. RANKL and OPG gene expression in the cells was analyzed by quantitative real-time polymerase chain reaction (qPCR) and their relative RANKL/OPG ratio was calculated. Both biofilm supernatants induced RANKL expression, but the subgingival caused a more pronounced up-regulation compared to the supragingival (10-fold at 6h and 100-fold at 24h). Changes in OPG expression in response to either biofilm were more limited. Accordingly, the subgingival biofilm caused a greater enhancement of the relative RANKL/OPG ratio (4-fold at 6h and 110-fold 24h). In conclusion, subgingival biofilms exhibit a stronger potency for inducing molecular mechanisms of bone resorption than supragingival biofilms, in line with their higher virulence nature for the development of periodontitis. AbstractPeriodontitis is an inflammatory condition that destroys the tooth supporting tissues, including the alveolar bone. It is triggered by polymicrobial biofilms attaching on tooth surfaces, which can be supragingival or subgingival. Bone resorption is triggered by RANKL and blocked by its soluble decoy receptor OPG, which are cytokines of the tumor necrosis factor ligand and receptor families, respectively. The present study aimed to comparatively investigate the effects of the Zürich in vitro supragingival and subgingival biofilm models, on RANKL and OPG gene expression in primary human GF cultures. The cells were challenged with the biofilms for up-to 24 hours. RANKL and OPG gene expression in the cells was analysed by qPCR and their relative RANKL/OPG ratio was calculated. Both biofilms induced RANKL expression, but the subgingival caused a more pronounced up-regulation compared to the supragingival (10-fold at 6 h and 100-fold at 24 h). Changes in OPG expression in response to either biofilm were more limited. Accordingly, the subgingival biofilm caused a greater enhancement of the relative RANKL/OPG ratio (4-fold at 6 h and 110-fold 24 h). In conclusion, subgingival biofilms exhibit a stronger potency for inducing molecular mechanisms of bone resorption than supragingival biofilms, in line with their higher virulence nature for the development of periodontitis.

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Section: Discussionsupporting

confidence: 88%

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

et al. 2011

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“…Such up-regulation of RANKL expression has also been reported during physiological dental root resorption in either cultured pulp cells or pulp tissues [3,5,36,51,53]. Our novel findings suggest that in uremic conditions, pulp cells may defensively express more RANKL to overcome its ossifying process.…”

Section: Discussionsupporting

confidence: 77%

Uremia Induces Dental Pulp Ossification but Reciprocally Inhibits Adjacent Alveolar Bone Osteogenesis

et al. 2015

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Uremic patients are predisposed to atrophy of the alveolar bone and narrowing of the dental pulp chamber. Such pulp chamber changes have only been diagnosed radiologically; however, this has not been supported by any pathological evidence. We used a uremic rat model with secondary hyperparathyroidism induced by 5/6 nephrectomy surgery and high-phosphate diet to examine the dental pulp and adjacent alveolar bone pathology. In addition, we collected pulp tissues for real-time PCR. We found an opposite histopathological presentation of the ossified dental pulp and the osteomalacic adjacent alveolar bone. Furthermore, pulp cells with positive staining for Thy-1, a surrogate stem cell marker, were significantly reduced in the pulp of uremic rats compared to the controls, indicating a paucity of stem cells. This was further evidenced by the reduced pulp expression of dickkopf-1 (Dkk-1), a Wnt/β-catenin signaling inhibitor produced by mesenchymal stem cells. In contrast, expressions of receptor activator of nuclear factor κB ligand (RANKL) and RANK in uremic pulp were up-regulated, probably to counteract the ossifying process of uremic pulp. In conclusion, uremic pulp ossifications were associated with a paucity of stem cells and dysregulated Dkk-1 and RANKL signaling systems, further shifting the imbalance toward osteogenesis. Strategies to counteract such an imbalance may offer a potential therapeutic target to improve dental health in uremic patients, which warrants further interventional studies.

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“…A few recent reports of hydroxyapatite discs used to create multispecies biofilms determined levels of IL-1ß, IL-6, IL-8 (Guggenheim et al, 2009), and RANKL/OPG (Belibasakis et al, 2011) produced by epithelial cells, periodontal ligament cells, or dental pulp cells in response to biofilms with multiple species. Analysis of the data indicated an apparent increase in apoptosis and degradation of Il-1ß, IL-6, and IL-8 in this system.…”

Section: Discussionmentioning

confidence: 99%

Oral Epithelial Cell Responses to Multispecies Microbial Biofilms

et al. 2013

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This report describes the use of a novel model of multispecies biofilms to stimulate profiles of cytokines/chemokines from oral epithelial cells that contribute to local inflammation in the periodontium. Streptococcus gordonii (Sg)/S. oralis (So)/S. sanguinis (Ss) and Sg/Fusobacterium nucleatum (Fn)/Porphyromonas gingivalis (Pg) biofilms elicited significantly elevated levels of IL-1α and showed synergistic stimulatory activity compared with an additive effect of the 3 individual bacteria. Only the Sg/Actinomyces naeslundii (An)/Fn multispecies biofilms elicited IL-6 levels above those of control. IL-8 was a primary response to the Sg/An/Fn biofilms, albeit the level was not enhanced compared with a predicted composite level from the monospecies challenges. These results represent some of the first data documenting alterations in profiles of oral epithelial cell responses to multispecies biofilms.

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Oral biofilm challenge regulates the RANKL-OPG system in periodontal ligament and dental pulp cells

Cited by 39 publications

References 35 publications

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

Uremia Induces Dental Pulp Ossification but Reciprocally Inhibits Adjacent Alveolar Bone Osteogenesis

Oral Epithelial Cell Responses to Multispecies Microbial Biofilms

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