Yamamoto M
Second Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Kyushu University, Fukuoka.
Fukuoka Igaku Zasshi. 1994 Mar;85(3):78-90.
The effect of malocclusion induced by increase in unilateral occlusal vertical dimension on the articular cartilage of rat mandibular condyle was histologically and immunohistologically examined. WKA rats (8 weeks) were divided into three group A: untreated (control) rats, group B: rats forced to mouth open just for 20 min, and group C: rats given malocclusion by putting the 1 mm diameter wire on the right upper molar continuously. After treatment, each rat was sacrificed periodically up to 9 weeks, and the morphological changes of condylar cartilage (articular, embryonic and transitional zones of cartilage layer) were histologically investigated. The thickness of articular cartilage in all groups was decreased in a time-dependent manner (up to 9 weeks after treatment). In group C rats, whose articular cartilage was thinnest in three groups, the reduced thickness of cartilage in the non-treated side (the left side) was same as that in the treated side which was presented with excessive molar contact. But, its occurrence in the treated side was seen 2 weeks earlier than that in the non-treated side. Even in group B rats which were only forced to open the mouth for 20 min without setting of permanent malocclusion, the thickness of condylar cartilage was decreased more than that of group A rats. When the condylar cartilages of all three groups were immunohistologically examined with anti-interleukin-1 (IL-1) antibody in order to investigate the pathophysiological involvement of IL-1, which is well-known catabolic factor to cartilage, some chondrocytes in articular cartilage were positively stained. The ratio of IL-1 positive cells increased time-dependently. IL-1-producing cells in group B and the non-treated side of group C reached to the maximal ratio at the same time when the condylar cartilage markedly decreased in thickness. However, the ratio of IL-1-positive chondrocytes in the treated side of group C was maximal four weeks after the decrease of cartilage thickness. In respect with the size of cells in cartilage, the occurrence of decreased thickness in condylar cartilage corresponded to that of the reduction of cellular size, especially in the embryonic zone of group C. These results described above suggest that malocclusion, unilateral immature occlusion, can induce the thinning of condylar cartilage which may result from the reducing size of articular chondrocytes (differentiated chondrocytes) and the accompanying decreased cartilage matrix. This change of cartilage may be caused by IL -1 that articular chondrocyte seemed to produce.(ABSTRACT TRUNCATED AT 400 WORDS)
通过组织学和免疫组织化学方法，研究了单侧咬合垂直距离增加所致错牙合对大鼠下颌髁突关节软骨的影响。将8周龄的WKA大鼠分为三组：A组为未处理（对照）大鼠；B组为仅强迫张口20分钟的大鼠；C组为在上颌右侧磨牙持续放置直径1mm金属丝造成错牙合的大鼠。处理后，在9周内定期处死每只大鼠，组织学观察髁突软骨（软骨层的关节、胚胎和过渡带）的形态变化。所有组的关节软骨厚度均呈时间依赖性降低（处理后9周内）。在三组中关节软骨最薄的C组大鼠中，未处理侧（左侧）软骨厚度的降低与存在过度磨牙接触的处理侧相同。但是，处理侧软骨厚度降低的出现比未处理侧早2周。即使在仅强迫张口20分钟而未造成永久性错牙合的B组大鼠中，髁突软骨厚度的降低也比A组大鼠更明显。为了研究白细胞介素-1（IL-1）（一种众所周知的软骨分解因子）的病理生理作用，用抗IL-1抗体对所有三组的髁突软骨进行免疫组织化学检测，发现关节软骨中的一些软骨细胞呈阳性染色。IL-1阳性细胞比例呈时间依赖性增加。B组和C组未处理侧产生IL-1的细胞在髁突软骨厚度明显降低时同时达到最大比例。然而，C组处理侧IL-1阳性软骨细胞的比例在软骨厚度降低4周后达到最大。关于软骨细胞大小，髁突软骨厚度降低的出现与细胞大小减小的出现相对应，尤其是在C组的胚胎带。上述结果表明，错牙合，单侧未成熟咬合，可导致髁突软骨变薄，这可能是由于关节软骨细胞（分化的软骨细胞）大小减小以及随之而来的软骨基质减少所致。软骨的这种变化可能是由关节软骨细胞似乎产生的IL-1引起的。（摘要截断于400字）
