The Effect of Cigarette Smoking And Low-Level Laser Irradiation in RANK/RANKL/OPG Expression

Abstract

The objective of this study was to investigate the effects of low-level laser therapy (LLLT) and cigarette smoke on alveolar socket osteoclastogenesis signaling after tooth extraction, in rats. Sixty male Wistar rats were randomly assigned to four groups with 15 animals each: Control Group (with right maxillary molar extraction - ME), Experimental I (with ME and LLLT), Experimental II (with ME and cigarette smoke) and Experimental III group (with ME, LLLT and cigarette smoke). Euthanasia was performed at 3, 7 and 14 days postoperative. qRT-PCR was used to evaluate expression of Tnfrsf11a (RANK), Tnfsf11 (Rankl) and Tnfrsf11b (OPG). Data were submitted to statistical analysis using two-way ANOVA followed by Bonferroni test (α=0.05). There was an upregulation of RANK, RANKL and OPG genes over all the time of healing in Exp I group compared to control group. Exp II group showed a decreased expression of all genes over time, whereas Exp III genes expression were higher than Exp II values but lower than Control and Exp I values over time. The results of this study concluded that the LLLT had a positive effect, whereas cigarette smoke had a negative effect on RANK, RANKL and OPG gene expression in bone remodeling process.

Physical activity and Mediterranean diet as potential modulators of osteoprotegerin and soluble RANKL in gBRCA1/2 mutation carriers: results of the lifestyle intervention pilot study LIBRE-1

“…Multivariate regression models also showed that cigarette smoking might influence the change of sRANKL in the course of the study. It has been shown that smoking can induce the expression of RANKL mRNA [ 67 ] and increases the sRANKL/OPG ratio by promoting inflammatory cytokines [ 68 ]. In a large case–control study it was demonstrated that cigarette smoking increased the risk for BC in g BRCA1/2 mutation carriers [ 69 ] for which sRANKL/OPG system might present a molecular mechanism of action.…”

Skeletal System Biology and Smoke Damage: From Basic Science to Medical Clinic

“…Based on the findings of Kim and colleagues, the effect is dose-dependent—at low concentrations, nicotine appears to have a stimulating effect on osteoblast proliferation, whereas at higher concentrations, the effect is inhibitory [ 43 ]. Cigarette smoke also exerts a direct effect on bone by altering bone-related factors involved in the regulation of osteoclastogenesis, such as the receptor activator of nuclear factor kappa-B ligand (RANKL)/receptor activator of nuclear factor kappa-B (RANK)/osteoprotegerin (OPG) system [ 44 , 45 , 46 ]. RANKL, released by osteoblasts, binds its receptor located on the surface of osteoclast precursor cells, promoting their differentiation and triggering bone resorption, whereas OPG, also released by osteoblasts, interacts with RANK, preventing the binding with its ligand and inhibiting the activity and proliferation of osteoclasts [ 47 ].…”

Low-level laser therapy (LLLT) improves alveolar bone healing in rats

“…The dental alveolus was curetted and abundantly irrigated, aiming for removal of residual fragments of hard and soft tissues that could interfere with healing. The molar was extracted in each rat with a dental explorer adapted to rat molars with a gentle buccolingual movement [9].…”

“…Irradiation was performed immediately after tooth extraction and daily for 3 consecutive days more, corresponding to the dosage of 54 J/cm 2 per day (total dosage of 216 J/cm 2 which corresponds to 4 dosages), lasting 42 s on each application with close contact with the cervical region of the dental alveolus surface. These conditions had been determined by previous experiments [9,21]. The treatment protocol for the sham groups (control group) was the same as for the experimental group, except that the laser device was not switched on [21].…”

“…Biostimulatory effects of low-level laser therapy (LLLT), a noninvasive treatment for inflammatory and pain issues, have been evaluated for alveolar bone repair, in particular, the acceleration of bone regeneration [1] in different treatments of the maxillofacial complex [9], due to the increase of mitotic activity of the epithelial cells [10] and changes in capillary density [11] increasing the local microcirculation [12], and, mainly, it increases the synthesis of collagen [13,14]. Numerous laser devices with different wavelengths, including helium-neon (HeNe 632.8 nm), gallium-aluminum-arsenide (GaAlAs 805 nm), and gallium-arsenide (GaAs 904 nm), have been used with different treatment protocols [2,[15][16][17].…”