Reinhardt Richard A, Lee Hsi-ming, Schmid Marian, Payne Jeffrey B, Golub Lorne
Departments of Surgical Specialties and Oral Biology, University of Nebraska Medical Center College of Dentistry, 40th and Holdrege Streets, Lincoln, NE 68583, USA.
J Oral Maxillofac Surg. 2005 Oct;63(10):1455-60. doi: 10.1016/j.joms.2005.05.319.
The aim of this pilot study was to determine the relationship between gelatinase (MMP-9 and MMP-2) markers of soft tissue inflammation/turnover at the bone/soft tissue interface and bone turnover (osteocalcin [OC], pyridinoline cross-linked carboxyl-terminal telopeptide of type 1 collagen [ICTP], and bone fill) during healing of an alveolar bone defect.
Ten subjects undergoing oral surgery had a 5 x 5-mm trephine defect created on an edentulous ridge and were sampled at the bone/soft tissue interface at baseline (prior to flap reflection), 2 weeks and 12 weeks postsurgery, using a novel bone wash device. Recovered irrigants were analyzed for MMP-9 and MMP-2 by gelatin zymography, OC and ICTP with radioimmunoassays, and albumin (ALB; to normalize markers for blood content) with a sandwich enzyme-linked immunosorbent assay. Bone fill at 12 weeks was analyzed by radiographic absorptiometry.
All markers of enzymatic activity and bone turnover varied significantly across time (P < or = .03), with bone turnover markers OC and ICTP decreasing between baseline and 2 weeks, and MMP-9 and MMP-2 increased. Measures generally returned to near baseline levels after 12 weeks. MMP-9 versus MMP-2 (r = 0.97, P < .0001) and OC versus ICTP (r = 0.38, P = .048) were correlated with each other, while MMP-9 and MMP-2 were negatively correlated with ICTP (r = -0.48, P = .011 and r = -0.62, P = .006, respectively). MMP-9 was negatively correlated with subsequent bone fill (r = -0.63, P = .07).
Bone wash sampling showed that gelatinase activity at 2 weeks following creation of an alveolar defect appeared to decrease bone turnover and eventual bone fill, suggesting benefits for anti-MMP therapy during wound healing.
本初步研究的目的是确定牙槽骨缺损愈合过程中，骨/软组织界面处软组织炎症/更新的明胶酶（基质金属蛋白酶-9和基质金属蛋白酶-2）标志物与骨更新（骨钙素[OC]、I型胶原吡啶啉交联羧基末端肽[ICTP]和骨填充）之间的关系。
10名接受口腔手术的受试者在无牙嵴上制作一个5×5毫米的环钻缺损，并在基线（翻瓣前）、术后2周和12周时，使用一种新型骨冲洗装置在骨/软组织界面进行采样。回收的冲洗液通过明胶酶谱法分析基质金属蛋白酶-9和基质金属蛋白酶-2，通过放射免疫分析法分析骨钙素和I型胶原吡啶啉交联羧基末端肽，通过夹心酶联免疫吸附测定法分析白蛋白（ALB；用于标准化血液含量的标志物）。12周时的骨填充通过放射吸收测定法进行分析。
所有酶活性和骨更新标志物随时间有显著变化（P≤0.03），骨更新标志物骨钙素和I型胶原吡啶啉交联羧基末端肽在基线和2周之间下降，而基质金属蛋白酶-9和基质金属蛋白酶-2增加。12周后各项指标通常恢复到接近基线水平。基质金属蛋白酶-9与基质金属蛋白酶-2（r = 0.97，P < 0.0001）以及骨钙素与I型胶原吡啶啉交联羧基末端肽（r = 0.38，P = 0.048）相互相关，而基质金属蛋白酶-9和基质金属蛋白酶-2与I型胶原吡啶啉交联羧基末端肽呈负相关（分别为r = -0.48，P = 0.011和r = -0.62，P = 0.006）。基质金属蛋白酶-9与随后的骨填充呈负相关（r = -0.63，P = 0.07）。
骨冲洗采样显示，牙槽骨缺损形成后2周时的明胶酶活性似乎会降低骨更新和最终的骨填充，这表明在伤口愈合期间进行抗基质金属蛋白酶治疗有益。
