Clinical measurements of periodontitis.
Clinical measurements of periodontitis.
复制标题
牙周炎的临床测量。
DOI：
10.1111/j.1600-051x.1986.tb01489.x
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发表时间：
1986
影响因子：
6.7
通讯作者：
Goodson,JM
中科院分区：
文献类型：
--
作者：
Goodson,JM
牙周炎的临床测量历来集中在牙周炎作为一个缓慢的，连续的过程，强调牙周袋的静态条件的测量的概念。在未治疗的受试者的附着丧失的纵向测量的基础上的观察表明，牙周破坏发生在短期的离散事件。基于这些研究，有人认为慢性牙周病是通过一系列随机发作进行的。牙周炎部位被认为存在于2种状态，即疾病活动性或非活动性。在疾病活动期间，站点的可探测深度增加，而在非活动状态期间，探测深度没有显著变化。从时间序列数据中检测牙周部位的变化已经通过3种分析方法解决：回归，运行中位数和公差。56名受试者的48064个部位的重复测量值之间差异的标准差为0.7727 mm。根据该估计值，计算出的单次测量值的标准差为0.5464 mm，2次测量值的平均值为0.386 mm。回归（p=0.028）、运行中位数（p=0.000025）和公差（p=0.00012）方法的I类错误均足够低，认为报告的观察结果不太可能由方法学错误解释。回归（p=0.446）、运行中位数（p =0.152）和容许误差（p =0.068）方法的II型误差估计值表明，这些方法未检测到相当一部分疾病活动位点。组内相关系数是根据105例患者的8,130个位点的附着水平变化计算的。通过该分析，7%的变化与受试者相关，93.3%与个体部位相关，表明牙周部位的附着水平变化具有高度的统计独立性。连续附件水平测量内的自相关计算，发现低（0.081在22名受试者和0.099在45名受试者），表明计算的方差没有系统性低估，由于数据集内的自相关。未能表现出与偶发性附着丧失相关性的临床测量包括牙龈发红、探诊出血、化脓、龈上菌斑和暗视野显微镜下细菌计数。与偶发性附着丧失相关的临床测量包括牙槽嵴骨的丧失和特定细菌种类的存在。在一项治疗快速进展性牙周炎的研究中，97.3%的非活动部位对治疗无效，而37.3%的疾病活动部位在全身四环素Widman瓣治疗后增加了3 mm或更多。这一观察结果表明，一般来说，只有疾病活动部位对治疗有反应。由于非活动中心（95-97%）的数量大大超过活动中心（3-5%），因此将其纳入临床试验有助于稀释治疗反应。基于这些研究结果，似乎希望未来的临床试验被诊断为牙周病活跃的网站进行。疾病活动性的检测出现中央牙周炎的临床测量。使用放射学方法来评估人体临床试验，虽然理论上是合理的，但尚未得到令人信服的证明。此时，测量活动性疾病的唯一实用方法是从重复依恋水平之间的差异。
Clinical measurement of periodontitis has historically focused on the concept of periodontitis as a slow, continuous process which has emphasized measurements of the static condition of periodontal pockets. Observations based on longitudinal measurement of attachment loss in untreated subjects have indicated that periodontal destruction occurs in discrete episodes of short duration. Based on these studies, it has been suggested that chronic periodontal disease proceeds through a series of random episodic attacks. Periodontal sites are considered as existing in 2 states, either disease active or inactive. During periods of disease activity, sites increase in their probeable depth, whereas during the inactive state, no significant change in probing depth can be detected. The detection of changes at periodontal sites from time series data has been addressed by 3 analytical procedures: regression, running medians, and tolerance. The standard deviation of differences between replicate measurements of48, 064 sites for 56 subjects was 0.7727 mm. From this estimate, the computed standard deviation for a single measurement was 0.5464 mm and for the mean of 2 measurements was 0.386 mm. The expected error rates of each method have been estimated by computer simulation. The type‐I error for the regression (p=0.028), running median (p=0.000025), and tolerance (p=0.00012) methods were all sufficiently low to consider it unlikely that reported observations could be accounted for by methodologic error. The estimated type‐II error for the regression (p=0.446), running medianp=0.152), and tolerancep=0.068) methods suggests that a substantial fraction of disease active sites was not detected by these methods.Several data set properties have been investigated. Intraclass correlation coefficients were computed from attachment level changes on8,130 sites in 105 patients. By this analysis, 7% of the variation was associated with the subject and 93.3% with the individual sites, indicating that attachment level changes at periodontal sites exhibit a high degree of statistical independence. Autocorrelation within sequential attachment level measurements was computed and found low (0.081 in 22 subjects and 0.099 in 45 subjects), indicating that computed variance is not systematically underestimated due to autocorrelation within the data set. Clinical measurements which have failed to exhibit association with episodic attachment loss include gingival redness, bleeding on probing, suppuration, supragingival plaque, and darkfield microscopic bacterial counts. Clinical measurements which have been associated with episodic attachment loss include loss of alveolar crestal bone and the presence of specific bacterial species. In a study of treatment for rapidly advancing periodontitis, 97.3% of inactive sites failed to respond to therapy, whereas 37.3% of disease active sites gained 3 mm or more following Widman flap therapy with systemic tetracycline. This observation indicates that, in general, only disease active sites respond to treatment. Since inactive sites (95–97%) greatly outnumber active sites (3–5%), their inclusion in clinical trials serves to dilute the treatment response. Based on these findings, it seems desirable that clinical trials of the future be conducted on periodontal sites diagnosed as disease active.Detection of disease activity appears central to the clinical measurement of periodontitis. The use of radiographic methods to evaluate human clinical trials, although theoretically sound, has not yet been convincingly demonstrated. At this time, the only practical means to measure active disease is from differences between repeated attachment level …