Bisphosphonates Induce Senescence in Normal Human Oral Keratinocytes
@article{Kim2011BisphosphonatesIS, title={Bisphosphonates Induce Senescence in Normal Human Oral Keratinocytes}, author={Reuben H Kim and Rachel S. Lee and D Williams and S Bae and Jessica Woo and Mark B. Lieberman and J-e Oh and Qinghua Dong and K. H. Shin and M. K. Kang and No-Hee Park}, journal={Journal of Dental Research}, year={2011}, volume={90}, pages={810 - 816}, url={https://api.semanticscholar.org/CorpusID:37337548} }
Analysis of data indicates that premature senescence of oral mucosal cells and subsequent defective soft-tissue wound healing might be partly responsible for the development of BRONJ in individuals receiving PAM or other BPs.
85 Citations
The Senescence Effect of Zoledronate on Three-Dimensional Oral Mucosa Model
- 2022
Medicine
This study suggests that ZOL may impair healing at multiple types of tissues, originally from keratinocytes, by the deleterious effects of the senescence-associated inflammatory response.
Microarray Gene Expression Profiling of Bisphosphonate-Treated Normal Human Oral Keratinocytes
- 2014
Medicine, Biology
It is demonstrated that inhibition of NHOK proliferation by BPs is, in part, mediated by suppressing CCNA2 expression at the transcriptional level, which may explain the underlying mechanisms of soft tissue toxicity by B Ps.
Bisphosphonate inhibits the expression of cyclin A2 at the transcriptional level in normal human oral keratinocytes
- 2017
Medicine
The findings of this study demonstrate that the inhibition of NHOK proliferation is mediated, at least in part, by the suppression of cyclin A2 expression at the transcriptional level, which may explain the underlying mechanisms of soft tissue toxicity by N-BPs.
at the level in normal human oral keratinocytes.
- 2017
Medicine, Biology
The findings of this study demonstrate that the inhibition of NHOK proliferation is mediated, at least in part, by the suppression of cyclin A2 expression at the transcriptional level, which may explain the underlying mechanisms of soft tissue toxicity by N-BPs.
Alendronate impairs epithelial adhesion, differentiation and proliferation in human oral mucosa.
- 2014
Medicine
The results show that epithelial adhesion, TD and proliferation are affected by ALN therapeutic doses in clinically healthy human oral mucosa.
Effect of low-level laser therapy on oral keratinocytes exposed to bisphosphonate
- 2013
Environmental Science, Medicine
Alendronate inhibits keratinocyte viability, expression of IL-8, VEGF, and collagen type I which are intimately related to healing events and cell migration while promoting apoptosis, and the utility of LLLT in partially overcoming the inhibitory effects of this bisphosphonate is demonstrated.
Synthetic Hydroxyapatite Inhibits Bisphosphonate Toxicity to the Oral Mucosa In Vitro
- 2020
Medicine, Materials Science
Results demonstrate hydroxyapatite granules protected oral soft tissues from damage caused by bisphosphonate exposure and suggest their potential to prevent MRONJ in at-risk patients.
In vitro Effect of Geranylgeraniol (GGOH) on Bisphosphonate-Induced Cytotoxicity of Oral Mucosa Cells
- 2022
Medicine
GGOH does not have therapeutic potential for bisphosphonate-induced soft tissue toxicity in MRONJ and the use of GGOH as an MRONj treatment should be strongly reconsidered.
Chronic alendronate therapy impairs epithelial morphology and homeostasis in the human oral mucosa
- 2012
Medicine
For the first time, epithelial homeostasis in human oral mucosa is profoundly affected by nitrogen containing BPs, confirming previous in vitro studies and strongly supporting the need of further investigation on the molecular mechanisms involved in ONJ pathogenesis.
33 References
Is Zoledronate Toxic to Human Periodontal Fibroblasts?
- 2010
Medicine
Analysis of data suggests that the cytotoxic responses of periodontal fibroblasts require high concentrations of zoledronate and depend on the in vitro experimental conditions, and whether these findings translate into soft-tissue damage will require further investigation.
Effect of zoledronic acid on oral fibroblasts and epithelial cells: a potential mechanism of bisphosphonate‐associated osteonecrosis
- 2009
Medicine
The potential for soft tissue injury as an initiating/potentiating event for osteonecrosis through the induction of a gene‐regulated apoptotic process is supported.
Senescence-associated genes in normal human oral keratinocytes.
- 2003
Biology, Medicine
Regulation of apoptosis by p53 in UV-irradiated human epidermis, psoriatic plaques and senescent keratinocytes
- 2002
Biology, Environmental Science
UV-light induces DNA damage in human epidermal KCs triggering p53 activation, and subsequent apoptosis involving distinct cell layers and kinetics, which depends not only on the location within various layers of epidermis and levels of p53, but may also involve p53activation via post-translational modifications.
Bmi-1 extends the life span of normal human oral keratinocytes by inhibiting the TGF-beta signaling.
- 2010
Biology, Medicine
The Matricellular Protein CCN1/CYR61 Induces Fibroblast Senescence and Restricts Fibrosis in Cutaneous Wound Healing
- 2010
Medicine, Biology
Fibroblast senescence is a CCN1-dependent wound healing response in cutaneous injury that functions to curb fibrosis during tissue repair.
Fibroblasts cultured from venous ulcers display cellular characteristics of senescence.
- 1998
Medicine, Biology
The treatment of bisphosphonate-associated osteonecrosis of the jaws with bone resection and autologous platelet-derived growth factors.
- 2007
Medicine
Treatment of refractory BON with a combination of marginal resection and PDGF has shown favorable results, including complete wound healing in most patients, and may be a useful alternative to existing treatment strategies.