Topical sodium alendronate combined or not with photodynamic therapy as an adjunct to scaling and root planing: Histochemical and immunohistochemical study in rats.

OBJECTIVE: The purpose of this study was to evaluate influence of topical sodium alendronate (ALN), photodynamic therapy (aPDT), or a combination thereof as adjuvant to scaling and root planing (SRP) in the treatment of experimental periodontitis in rats. BACKGROUND: Therapeutic protocols to control periodontitis progression that aim to equalize bacterial action and load with tissue immune response are well addressed in current scientific research. METHODS: Experimental periodontitis was induced in 96 rats with a ligature around the mandibular left first molar. After 7 days, ligature was removed and animals were treated according to the following experimental groups (n = 8): control-SRP plus saline solution; ALN-SRP plus ALN; aPDT-SRP plus methylene blue irrigation, followed by low-level laser therapy (LLLT); and ALN/aPDT-SRP plus ALN and methylene blue irrigation followed by LLLT. The animals were euthanized at 7, 15, and 30 days after treatments. Collagen maturation (picrosirius red staining) and immunohistochemical analyses (TRAP, RANKL and osteoprotegerin [OPG]) were performed. Data were submitted to statistical analysis (P < .05). RESULTS: At 7 days, group ALN presented a significantly higher number of TRAP-positive cells and percentage of immature collagen fibers than group ALN/aPDT, while group ALN/aPDT presented a significantly higher percentage of mature collagen fibers than group ALN. At 30 days, group ALN presented significantly lower percentage of immature collagen fibers and higher percentage of mature collagen fibers than control. CONCLUSION: It can be concluded that topical use of ALN coadjutant to SRP, alone or combined with aPDT, enhanced collagen maturation and reduced osteoclastogenesis during the healing of experimental periodontitis.

Chronic high glucose and insulin stimulate bone-marrow stromal cells adipogenic differentiation in young spontaneously hypertensive rats.

We evaluated whether genetic predisposition is sufficient to induce changes due to chronic high glucose (HG; 25 mmol/L) in the presence or absence of insulin (HGI; 10 µg/ml) on osteogenic differentiation and markers in bone-marrow mesenchymal stem cells (BMSCs) from young Wistar (WBMSCs) and spontaneous hypertensive rats (SBMSCs) without hypertension. HG suppressed osteogenic differentiation in both the strains, observed by mineralization inhibition and decreased levels of the osteogenic markers Runx2, osterix, osteopontin, and bone sialoprotein, compared to osteogenic medium (OM) cells. In WBMSCs, the effects of HG were associated with the down regulation of ERK1/2 and up regulation of p38 activities; however, HGI did not revert the effects of HG on MAPK activities. Moreover, HG did not affect MAPK signaling in SBMSCs compared to that in OM. HGI increased mineralization in WBMSCs compared to that in OM, but not in SBMSCs. High expression of peroxisome proliferator-activated receptor-gamma and glucose transporter type 4 in OM could be related with the predisposition to adipogenic differentiation noted in SBMSCs and was confirmed by emergence of adipocyte-like cells by HGI treatment. Downregulation of p38 and upregulation of JNK activities were observed in both BMSCs treated with HGI compared to those treated by HG. Ma (osmotic control) also suppressed osteogenic differentiation in both the strains. In conclusion, we demonstrated that SBMSCs from young spontaneous hypertensive rats, without hypertension but with genetic and epigenetic predisposition, exhibited decreased osteoblastic differentiation under HG and HGI did not revert the effects of HG in SBMSCs but increased adipogenic differentiation.