Altıntepe Doğan Suat Serhan, Toker Hülya, Göze Ömer Fahrettin
Department of Periodontology, Faculty of Dentistry, Afyonkarahisar Health Sciences University, 03030 Afyonkarahisar, Turkey.
Department of Periodontology, Faculty of Gulhane Dentistry, Health Sciences University, 06018 Ankara, Turkey.
Biomedicines. 2024 Mar 19;12(3):684. doi: 10.3390/biomedicines12030684.
Periodontitis and post-menopausal osteoporosis include common chronic bone disorders worldwide, with similar etiopathogenetic events. This study evaluated the effect of systemic melatonin administration on the alveolar bone destruction of periodontitis progression in an experimental periodontitis model in osteoporotic rats.
Forty-four Wistar rats were randomly divided into six experimental groups: control (C; = 6); osteoporosis (O; = 6); ligated periodontitis (LP; = 8); osteoporosis- and periodontitis-induced (O+LP; = 8); osteoporosis- and periodontitis-induced through 30 mg/kg/day melatonin administration (ML30; = 8); and osteoporosis- and periodontitis-induced through 50 mg/kg/day melatonin administration (ML50; = 8). The rats underwent bilateraloophorectomy and were maintained for 4 months to induce osteoporosis. After 4 months, 4-0 silk ligatures were placed submarginally around the mandibular first molar of each rat to induce experimental periodontitis, and melatonin was administered in the ML30 and ML50 groups for 30 days. Changes in alveolar bone levels were clinically measured, and tissues were histopathologically examined.
Osteoclastic activity in the LP and O+LP groups was significantly higher than in the other groups ( < 0.05), but was similar in the C, O, and ML30 groups ( > 0.05). RANKL activity was the highest in the O+LP group, while melatonin decreased RANKL activity in the melatonin-administered groups ( < 0.05). Systemically administered melatonin significantly decreased alveolar bone loss in the ML30 and ML50 groups compared with that in the periodontitis groups ( < 0.05).
Melatonin inhibited alveolar bone destruction by decreasing the RANKL expression and inflammatory cell infiltration and increased osteoblastic activity in a rat model with osteoporosis and periodontitis.
牙周炎和绝经后骨质疏松症是全球常见的慢性骨疾病，具有相似的发病机制。本研究在骨质疏松大鼠实验性牙周炎模型中评估了全身给予褪黑素对牙周炎进展过程中牙槽骨破坏的影响。
44只Wistar大鼠随机分为6个实验组：对照组（C；n = 6）；骨质疏松组（O；n = 6）；结扎性牙周炎组（LP；n = 8）；骨质疏松合并牙周炎组（O + LP；n = 8）；通过每天给予30 mg/kg褪黑素诱导骨质疏松合并牙周炎组（ML30；n = 8）；通过每天给予50 mg/kg褪黑素诱导骨质疏松合并牙周炎组（ML50；n = 8）。大鼠接受双侧卵巢切除术并维持4个月以诱导骨质疏松。4个月后，在每只大鼠下颌第一磨牙龈下放置4-0丝线结扎以诱导实验性牙周炎，ML30组和ML50组给予褪黑素30天。临床测量牙槽骨水平变化，并进行组织病理学检查。
LP组和O + LP组的破骨细胞活性显著高于其他组（P < 0.05），但C组、O组和ML30组相似（P > 0.05）。RANKL活性在O + LP组中最高，而褪黑素降低了给予褪黑素组中的RANKL活性（P < 0.05）。与牙周炎组相比，全身给予褪黑素显著降低了ML30组和ML50组的牙槽骨丢失（P < 0.05）。
在骨质疏松合并牙周炎大鼠模型中，褪黑素通过降低RANKL表达和炎症细胞浸润抑制牙槽骨破坏，并增加成骨细胞活性。
