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Objectives The aim of the current clinical trial was to evaluate if the oral supplementation of melatonin after nonsurgical periodontal therapy (NSPT) determined a better periodontal healing than NSPT alone, in patients affected by untreated severe periodontitis. Background Melatonin's anti‐inflammatory, antioxidant and immunomodulatory capacities, together with its pharmacokinetic and pharmacodynamic profiles are key characteristics that justify the therapeutic use for the treatment of periodontitis. Methods This is a randomized, triple‐blind, placebo‐controlled study. Twenty patients were blindly randomized either to melatonin or placebo group. The melatonin group received NSPT and melatonin capsules 1 mg per day for 1 month, while the placebo, NSPT, and placebo capsules for 1 month. The patients were evaluated at baseline and 6 months after. Mean change from baseline probing depth (PD) was the primary outcome; site of probing was used as unit of analysis; FMBS (%) and FMPS (%) were also calculated. Mann‐Whitney test was used to evaluate statistical significance (α = 0.05). Results Melatonin was well tolerated by all patients. Both treatments were effective in reducing PD, but no statistical difference was found when comparing posttreatment PD (probing all sites), P = .62. When considering the primary outcome, melatonin administration resulted in greater mean PD change at 6 months if compared to control group: for 4‐5 mm sites 1.86 (0.81) vs 1.04 (0.69), P = .00001 and for sites >5 mm 3.33 (1.43) vs 2.11 (0.96), P = .00012. No difference was found for FMBS and FMPS. Conclusion Current study, within its limitations, concluded that oral administration of melatonin (1 mg per day for 30 days) after one‐stage full mouth NSPT determined a greater change from baseline PD if compared to NSPT alone, in untreated stage III periodontitis. This could provide a non‐pharmacological support to improve periodontal healing of periodontal sites after NSPT.

Our findings support the hypothesis that hydrophyte adaptive strategy variation reflects fundamental trade-offs in economics and size that govern all plants, and that hydrophyte adaptive strategies can be directly compared with terrestrial species by combining leaf economics and size traits.

Human mesenchymal stem cells (MSCs) have the potential to differentiate into cells of connective tissue lineages, including bone, cartilage, fat, muscle and also neurons. In our study we have examined the phenotypic profile of human adipose tissue-derived stem cells (hASCs) and compared different osteogenic-inductive media to assess hASC differentiation. Cells were enzymatically isolated from adipose tissues derived by liposuction from several adult human donors, purified and then expanded in culture. We obtained an abundant yield of hASCs with a constant proliferative trend, a doubling time of about 68 h and a mild variable clonogenic capacity. At passage 4, hASCs expressed MSC-related cell surface antigens (CD13, CD105, CD54, CD90, CD44), and subsequently hASCs were induced to differentiate into the osteogenic lineage for at least 3 weeks of culture in two distinct media, OM1 and OM2, differing in dexamethasone and ascorbic acid concentrations. Osteogenic differentiation of OM1-and OM2-cultured cells was assessed by evaluating cell morphology, osteopontin expression, alkaline phosphatase activity and calcium deposition. OM2 medium showed a higher osteogenic potential than OM1, as assessed by increased levels of calcium deposition, alkaline phospatase activity and osteopontin expression in comparison with OM1-differentiated cells. We conclude that hASCs efficiently differentiate into osteogenic lineage, particularly when cultured in inductive medium supplemented with 10 nM dexamethasone and 150 µM ascorbic acid.

Tissue engineering is now contributing to new developments in several clinical fields, and mesenchymal stem cells derived from adipose tissue (hASCs) may provide a novel opportunity to replace, repair and promote the regeneration of diseased or damaged musculoskeletal tissue. Our interest was to characterize and differentiate hASCs isolated from twenty-three donors. Proliferation, CFU-F, cytofluorimetric and histochemistry analyses were performed. HASCs differentiate into osteogenic, chondrogenic, and adipogenic lineages, as assessed by tissue-specific markers such as alkaline phosphatase, osteopontin expression and deposition of calcium matrix, lipid-vacuoles formation and Glycosaminoglycans production. We also compared osteo-differentiated hASCs cultured on monolayer and loaded on biomaterials routinely used in the clinic, such as hydroxyapatite, cancellous human bone fragments, deproteinized bovine bone granules, and titanium. Scaffolds loaded with pre-differentiated hASCs do not affect cell proliferation and no cellular toxicity was observed. HASCs tightly adhere to scaffolds and differentiated-hASCs on human bone fragments and bovine bone granules produced, respectively, 3.4- and 2.1-fold more calcified matrix than osteo-differentiated hASCs on monolayer. Moreover, both human and deproteinized bovine bone is able to induce osteogenic differentiation of CTRL-hASCs. Although our in vitro results need to be confirmed in in vivo bone regeneration models, our data suggest that hASCs may be considered suitable biological tools for the screening of innovative scaffolds that would be useful in tissue engineering.