Oktay Sehkar, Chukkapalli Sasanka S, Rivera-Kweh Mercedes F, Velsko Irina M, Holliday L Shannon, Kesavalu Lakshmyya
Department of Periodontology, College of Dentistry, University of Florida, Gainesville, FL.
J Periodontol. 2015 Jan;86(1):137-45. doi: 10.1902/jop.2014.140302.
Periodontitis is a chronic, polymicrobial inflammatory disease that degrades connective tissue and alveolar bone and results in tooth loss. Oxidative stress has been linked to the onset of periodontal tissue breakdown and systemic inflammation, and the success of antiresorptive treatments will rely on how effectively they can ameliorate periodontal disease-induced oxidative stress during oral infection.
Rats were infected with polybacterial inoculum consisting of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, as an oral lavage every other week for 12 weeks. Daily subcutaneous injections of enoxacin, bis-enoxacin, alendronate, or doxycycline were administered for 6 weeks after 6 weeks of polybacterial infection in rats. The serum levels of oxidative stress parameters and antioxidant enzymes, including glutathione peroxidase, superoxide dismutase, and catalase, were evaluated in each of the infected, treated, and sham-infected rats.
Rats infected with the periodontal pathogens displayed a five-fold increase in the oxidative stress index compared with controls as a result of increased levels of serum oxidants and decreases in total antioxidant activity. The overall decrease in antioxidant activity occurred despite increases in three important antioxidant enzymes, suggesting an imbalance between antioxidant macromolecules/small molecules production and antioxidant enzyme levels. Surprisingly, the bone-targeted antiresorptives bis-enoxacin and alendronate inhibited increases in oxidative stress caused by periodontitis. Bis-enoxacin, which has both antiresorptive and antibiotic activities, was more effective than alendronate, which acts only as an antiresorptive.
To the best of the authors' knowledge, this is the first study to demonstrate that the increased oxidative stress induced by periodontal infection in rats can be ameliorated by bone-targeted antiresorptives.
牙周炎是一种慢性、多微生物炎症性疾病,会导致结缔组织和牙槽骨退化,进而导致牙齿脱落。氧化应激与牙周组织破坏和全身炎症的发生有关,抗吸收治疗的成功将取决于它们在口腔感染期间减轻牙周病诱导的氧化应激的效果。
大鼠每隔一周接受由牙龈卟啉单胞菌、具核梭杆菌和福赛坦氏菌组成的多菌接种物口腔灌洗,持续12周。在大鼠多菌感染6周后,每天皮下注射依诺沙星、双依诺沙星、阿仑膦酸盐或强力霉素,持续6周。对每组感染、治疗和假感染大鼠的氧化应激参数和抗氧化酶(包括谷胱甘肽过氧化物酶、超氧化物歧化酶和过氧化氢酶)的血清水平进行评估。
与对照组相比,感染牙周病原体的大鼠氧化应激指数增加了五倍,这是由于血清氧化剂水平升高和总抗氧化活性降低所致。尽管三种重要的抗氧化酶有所增加,但抗氧化活性总体下降,这表明抗氧化大分子/小分子的产生与抗氧化酶水平之间存在失衡。令人惊讶的是,骨靶向抗吸收剂双依诺沙星和阿仑膦酸盐抑制了牙周炎引起的氧化应激增加。具有抗吸收和抗生素活性的双依诺沙星比仅作为抗吸收剂的阿仑膦酸盐更有效。
据作者所知,这是第一项证明骨靶向抗吸收剂可改善大鼠牙周感染诱导的氧化应激增加的研究。