Subgingival plaque and loss of attachment in periodontosis as observed in autopsy material.
Subgingival plaque and loss of attachment in periodontosis as observed in autopsy material.
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在尸检材料中观察到牙周病中的龈下菌斑和附着丧失。
DOI：
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发表时间：
1976
期刊：
影响因子：
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通讯作者：
J. Waerhaug
中科院分区：
文献类型：
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作者：
J. Waerhaug
从临床角度来看，符合牙周病标准的6例尸检病例的组织切片进行了检查，目的是评估龈下菌斑在这种情况下附着丧失病因学中的作用。提出了以下有关意见：1。大多数情况下龈下菌斑不会钙化形成牙石。2.龈下菌斑的厚度在20和200 μ（0.02-0.2 mm）之间变化。3.在附着丧失的地方，从龈下菌斑的最顶端部分到上皮袖的最顶端点的距离在0.2和1.1 mm之间变化;从未发现该距离超过1.1 mm。这表明存在因果关系，菌斑是明显的原因。4.斑块周围的软组织存在非常严重的慢性炎症，导致胶原溶解。5.细胞浸润和胶原溶解可限于紧邻斑块的1至2 mm区域。在发炎区域和牙龈颊侧和舌侧的表面之间，可能存在相当宽的健康组织区域，其隐藏了在临床检查中观察不到的炎症症状。反过来，这可能会给临床医生留下这样的印象，即由于退行性变化，附着已经丢失和骨吸收。可以得出以下结论：在这6例“牙槽骨丢失与该年龄患者的局部病因因素所预期的严重不成比例”的病例中，没有形态学证据表明退行性变化是导致附着丧失的原因。相反，由龈下斑块引起的炎性变化占主导地位的组织病理学图片。
Histologic sections from six autopsy cases which from a clinical point of view fitted into the criteria of periodontosis were examined with the aim at evaluating the role of subgingival plaque in the etiology of the loss of attachment in this condition. The following pertinent observations were made: 1. The subgingival plaque in most instances was not calcified to form calculus. 2. The thickness of the subgingival plaque varied between 20 and 200 mu (0.02-0.2 mm). 3. Where loss of attachment had taken place, the distance from the most apical part of the subgingival plaque to the most apical point of the epithelial cuff varied between 0.2 and 1.1 mm; this distance was never found to be more than 1.1 mm. This would indicate a cause and effect relationship, the plaque being the obvious cause. 4. There was very severe chronic inflammation in the soft tissue bordering upon the plaque with resulting collagenolysis. 5. The cellular infiltration and the collagenolysis may be limited to a zone of 1 to 2 mm in the immediate vicinity of the plaque. Between the inflamed area and the surface of the gingivae buccally and lingually there may be a fairly wide zone of healthy tissue which hides the symptoms of inflammation from being observed on a clinical examination. In turn this could leave the clinician with the impression that attachment has been lost and bone resorbed because of degenerative changes. The following conclusions can be made: In these six cases of "alveolar bone loss vastly out of proportion to what one would expect from the local etiologic factors in the patient at that age" there was no morphologic evidence that degenerative changes were responsible for the loss of attachment. On the contrary inflammatory changes induced by the subgingval plaque dominated the histopathologic picture.