Komatsu Keiji, Matsuura Takanori, Suzumura Toshikatsu, Shibata Rune, Chen Po-Chun, Ogawa Takahiro
Weintraub Center for Reconstructive Biotechnology, UCLA School of Dentistry, Los Angeles, California 90095, United States.
Department of Lifetime Oral Health Care Sciences, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, 113-8549, Japan.
ACS Appl Bio Mater. 2025 May 19;8(5):4166-4185. doi: 10.1021/acsabm.5c00283. Epub 2025 Apr 18.
Bacterial invasion at the titanium-tissue interface causes peri-implant inflammation, posing challenges for implants in orthopedics, maxillofacial prosthetics, and dentistry. This study hypothesized that titanium surface decarbonization improves soft tissue cell adhesion and growth. One-minute vacuum ultraviolet (VUV) light treatment at 172 nm reduced surface carbon from 60% to 29% without altering surface topography, making surfaces hydrophilic and hydro-attractive. Human fibroblasts attached to VUV-treated surfaces 2-4 times more frequently than untreated surfaces, with an even greater increase on tilted and curved surfaces. Fibroblast proliferation rose 2-6 times, with an expedited G1-to-S phase transition. Cell retention under dislodging forces increased 2-5 times on VUV-treated surfaces. RNA sequencing showed upregulation of extracellular matrix production, growth factors, cell cycle progression, antioxidant defenses, and proteoglycan/glycosaminoglycan (GAG)-binding, alongside downregulation of the inflammatory response on VUV-treated titanium surfaces. An oxidative stress test showed minimal adverse effects from hydrogen peroxide on cells on VUV-treated surfaces, attributed to increased intracellular glutathione reserves. Enhanced adhesion on VUV-treated titanium was negated by treating the cells with GAG-cleaving enzymes. These findings demonstrate that VUV-mediated decarbonization enhances fibroblast attachment, proliferation, and adhesion by fostering homeostatic cellular phenotypes involving proteoglycan/GAG interactions and antioxidant defense, offering a strategy to improve the soft tissue sealing around titanium implants.
钛-组织界面处的细菌入侵会引发种植体周围炎症,这给骨科、颌面修复和牙科领域的植入物带来了挑战。本研究假设钛表面脱碳可改善软组织细胞的黏附与生长。172纳米的一分钟真空紫外线(VUV)光处理可将表面碳含量从60%降至29%,而不改变表面形貌,使表面具有亲水性和水吸引力。人成纤维细胞附着在经VUV处理的表面上的频率是未处理表面的2至4倍,在倾斜和弯曲表面上的增加更为显著。成纤维细胞增殖增加了2至6倍,G1期到S期的转变加快。在VUV处理过的表面上,在脱位力作用下细胞的保留率提高了2至5倍。RNA测序显示,在经VUV处理的钛表面上,细胞外基质产生、生长因子、细胞周期进程、抗氧化防御以及蛋白聚糖/糖胺聚糖(GAG)结合上调,同时炎症反应下调。氧化应激试验表明,过氧化氢对VUV处理表面上的细胞的不良影响最小,这归因于细胞内谷胱甘肽储备的增加。用GAG裂解酶处理细胞可消除经VUV处理的钛表面上增强的黏附作用。这些发现表明,VUV介导的脱碳通过促进涉及蛋白聚糖/GAG相互作用和抗氧化防御的稳态细胞表型,增强了成纤维细胞的附着、增殖和黏附,为改善钛植入物周围的软组织密封提供了一种策略。