Radaic Allan, Brody Hanna, Contreras Fernando, Hajfathalian Maryam, Lucido Luke, Kamarajan Pachiyappan, Kapila Yvonne L
Department of Orofacial Sciences, School of Dentistry, University of California San Francisco, San Francisco, CA 94143, USA.
Department of Radiology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Microorganisms. 2022 Jul 1;10(7):1336. doi: 10.3390/microorganisms10071336.
Peri-implantitis is characterized by chronic inflammation of the peri-implant supporting tissues that progressively and irreversibly leads to bone loss and, consequently, implant loss. Similar to periodontal disease, oral dysbiosis is thought to be a driver of peri-implantitis. However, managing peri-implantitis with traditional treatment methods, such as nonsurgical debridement or surgery, is not always successful. Thus, novel strategies have been proposed to address these shortcomings. One strategy is the use of probiotics as antimicrobial agents since they are considered safe for humans and the environment. Specifically, the probiotic produces nisin, which has been used worldwide for food preservation. The objective of this study was to determine whether nisin and the wild-type (WT) nisin-producing probiotic can disrupt oral pathogenic biofilms and promote a healthier oral microbiome within these oral biofilms on titanium discs. Using confocal imaging and 16S rRNA sequencing, this study revealed that nisin and WT probiotic disrupt oral pathogenic biofilms in a peri-implantitis setting in vitro. More specifically, nisin decreased the viability of the pathogen-spiked biofilms dose-dependently from 62.53 ± 3.69% to 54.26 ± 3.35% and 44.88 ± 2.98%, respectively. Similarly, 10 CFU/mL of WT significantly decreased biofilm viability to 52.45 ± 3.41%. Further, both treatments shift the composition, relative abundance, and diversity levels of these biofilms towards healthy control levels. A total of 1 µg/mL of nisin and 10 CFU/mL of WT were able to revert the pathogen-mediated changes in the Proteobacteria (from 80.5 ± 2.9% to 75.6 ± 2.0%, 78.0 ± 2.8%, and 75.1 ± 5.3%, respectively) and Firmicutes (from 11.6 ± 1.6% to 15.4 ± 1.3%, 13.8 ± 1.8%, and 13.7 ± 2.6%, respectively) phyla back towards control levels. Thus, nisin and its nisin-producing probiotic may be useful in treating peri-implantitis by promoting healthier oral biofilms, which may be useful for improving patient oral health.
种植体周围炎的特征是种植体周围支持组织的慢性炎症，这种炎症会逐渐且不可逆地导致骨质流失，进而导致种植体脱落。与牙周疾病类似，口腔生态失调被认为是种植体周围炎的一个驱动因素。然而，使用传统治疗方法（如非手术清创或手术）来治疗种植体周围炎并不总是成功的。因此，人们提出了新的策略来解决这些缺点。一种策略是使用益生菌作为抗菌剂，因为它们被认为对人类和环境都是安全的。具体而言，这种益生菌能产生乳酸链球菌素，该物质已在全球范围内用于食品保鲜。本研究的目的是确定乳酸链球菌素和产生乳酸链球菌素的野生型（WT）益生菌是否能破坏口腔致病生物膜，并在钛盘上的这些口腔生物膜中促进更健康的口腔微生物群。通过共聚焦成像和16S rRNA测序，本研究表明，在体外种植体周围炎环境中，乳酸链球菌素和WT益生菌能破坏口腔致病生物膜。更具体地说，乳酸链球菌素能剂量依赖性地降低接种病原体的生物膜的活力，分别从62.53±3.69%降至54.26±3.35%和44.88±2.98%。同样，10 CFU/mL的WT能将生物膜活力显著降低至52.45±3.41%。此外，两种处理方法都能使这些生物膜的组成、相对丰度和多样性水平朝着健康对照水平转变。总共1 µg/mL的乳酸链球菌素和10 CFU/mL的WT能够使变形菌门（分别从80.5±2.9%降至75.6±2.0%、78.0±2.8%和75.1±5.3%）和厚壁菌门（分别从11.6±1.6%增至15.4±1.3%、13.8±1.8%和13.7±2.6%）中由病原体介导的变化恢复到对照水平。因此，乳酸链球菌素及其产生乳酸链球菌素的益生菌可能通过促进更健康的口腔生物膜来治疗种植体周围炎，这可能有助于改善患者的口腔健康。
