Background/purposeMelatonin, at physiological concentrations, was previously found to inhibit proliferation and promote odontogenic differentiation in human dental pulp cells (hDPCs), but its effect on apoptosis is unclear. Our study aimed to investigate the effect of melatonin on the H2O2-mediated viability reduction and apoptosis in hDPCs.Materials and methodshDPCs were treated with H2O2 (0, 250, 500, 1000 μmol/L), melatonin (0, 10−12, 10−10, 10−8 mol/L), and melatonin with H2O2 for 24 h. CCK-8 assays were performed to evaluate cell viability. Apoptosis was measured by DAPI and Annexin V/propidium iodide staining. Intracellular reactive oxygen species (ROS) were measured by CellROX® staining and mitochondrial membrane potential (ΔΨm) was examined by JC-1 staining.ResultsH2O2 obviously decreased the viability of hDPCs in a concentration-dependent manner and melatonin alone also reduced viability by 16–20%. Melatonin was also found to enhance H2O2-induced toxicity in a concentration-dependent manner, and the highest physiological concentration of melatonin (10−8 mol/L) had the most obvious effect (P < 0.001). Treating H2O2-exposed hDPCs with melatonin significantly increased the ratio of apoptotic cells with condensed and deformed nuclei (P < 0.001), as well as the percentage of Annexin V-positive cells (P < 0.01). Furthermore, melatonin significantly increased intracellular ROS levels and induced the loss of ΔΨm in H2O2-exposed cells (P < 0.05).ConclusionOur results indicate that melatonin, at physiological concentrations, can enhance H2O2-induced apoptosis in hDPCs and increase H2O2-mediated ROS production and ΔΨm loss. Further studies are needed to investigate whether melatonin targets the mitochondrial death pathway during the process.
Cutaneous sinus tracts of dental origin are relatively rare, but frequently misdiagnosed. In this case report, we present a seven-year-old patient with a cutaneous lesion in the left submandibular region misdiagnosed by a physician as an abscess secondary to suppurative lymphadenitis, and thus incorrectly treated with surgery and systemic antibiotics. Following a detailed dental examination, the patient was correctly diagnosed with an odontogenic sinus tract from a periapical abscess of tooth 36. Treatment of the immature tooth was initiated with apexification combined with nonsurgical endodontic treatment. The cutaneous and the periapical lesions were all resolved after the treatment and there has been no recurrence during an eight-year follow-up.
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