Cellular source and tetracycline-inhibition of gingival crevicular fluid collagenase of patients with labile diabetes mellitus.
Cellular source and tetracycline-inhibition of gingival crevicular fluid collagenase of patients with labile diabetes mellitus.
复制标题
不稳定糖尿病患者龈沟液胶原酶的细胞来源和四环素抑制。
DOI：
10.1111/j.1600-051x.1992.tb00454.x
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发表时间：
1992
影响因子：
6.7
通讯作者：
Golub,LM
中科院分区：
文献类型：
--
作者：
Sorsa,T;Ingman,T;Suomalainen,K;Halinen,S;Saari,H;Konttinen,YT;Uitto,VJ;Golub,LM
不稳定型胰岛素依赖型糖尿病（DM）和局限性青少年牙周炎（LJP）患者的牙周组织加速破坏与中性粒细胞功能异常有关。我们最近发现，在牙龈沟液（GCF）的成人牙周炎患者的胶原酶主要来自中性粒细胞和中性粒细胞的胶原酶活性是更敏感的抑制四环素比胶原酶产生的成纤维细胞。本研究旨在探讨糖尿病患者龈沟液中胶原酶的细胞来源、激活和抑制情况，并与LJP龈沟液中胶原酶进行比较。我们发现的差异可能具有治疗意义。特异性强力霉素抑制试验显示，DM中的GCF胶原酶来源于中性粒细胞，而LJP中的酶主要来源于成纤维细胞。氧化剂次氯酸钠能有效激活DM患者GCF胶原酶，但对LJP患者无明显作用。与此相反，纤溶酶激活LJP GCF胶原酶，但不是糖尿病患者。在糖尿病患者的GCF中，50-60%的胶原酶以活性形式存在，而在LJP GCF中，该酶几乎完全以潜伏形式存在。结果表明，GCF的不稳定的糖尿病牙周炎患者的胶原酶主要来自中性粒细胞和四环素治疗可能是一种有效的辅助治疗，旨在控制这些患者的牙周崩溃。另一方面，在LJP中，由于成纤维细胞胶原酶的四环素耐药性，四环素类的抗胶原酶特性对于控制牙周组织破坏可能不太重要。
Accelerated periodontal tissue destruction in patients with labile insulin‐dependent diabetes mellitus (DM) and localized juvenile periodontitis (LJP) has been suggested to be related to functional abnormalities of neutrophils. We have recently found that collagenase in gingival crevicular fluid (GCF) of adult periodontitis patients is primarily derived from neutrophils and that neutrophil collagenase activity is more sensitive to inhibition by tetracyclines than collagenase produced by fibroblasts. This study is to characterize the cellular sources, activation and inhibition of collagenase in GCF of DM patients and to compare it with collagenase in LJP GCF. We found differences which may have therapeutic implications. Specific doxycycline inhibition tests revealed that GCF collagenase in DM is derived from neutrophils, whereas the enzyme in LJP originates primarily from fibroblasts. Oxidant, sodium hypochlorite activated efficiently GCF collagenase of DM but not LJP patients. In contrast, plasmin activated LJP GCF collagenase but not that of DM patients. In GCF of DM patients 50–60% of collagenase existed in an active form, whereas in LJP GCF, the enzyme was almost completely in a latent form. The results suggest that collagenase in GCF of periodontitis patients with labile DM is primarily derived from neutrophils and that tetracycline therapy may be an effective adjunct in treatment aimed at controlling the periodontal breakdown in these patients. On the other hand, in LJP the anti‐collagenase property of tetracyclines may be less important for control of periodontal tissue destruction because of the tetracycline‐resistance of fibroblast collagenase.