Diabetic periodontitis: possible lipid-induced defect in tissue repair through alteration of macrophage phenotype and function.
Diabetic periodontitis: possible lipid-induced defect in tissue repair through alteration of macrophage phenotype and function.
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糖尿病牙周炎：可能是脂质通过巨噬细胞表型和功能的改变引起组织修复缺陷。
DOI：
10.1111/j.1601-0825.1995.tb00187.x
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发表时间：
1995
期刊：
影响因子：
3.8
通讯作者：
Iacopino,AM
中科院分区：
文献类型：
--
作者：
Iacopino,AM
背景：糖尿病是美国的一个主要健康问题，影响着大约1300万人。历史上与这种情况有关的五种“经典”并发症是微血管病变、神经病变、肾病、微血管疾病和伤口愈合延迟。最近，随着糖尿病患者牙周病发病率和严重程度的增加，牙周病已被宣布为糖尿病的第六大并发症。糖尿病帕金森病的细胞和分子基础尚不清楚。背景：最近的证据表明，帕金森病和皮肤创面愈合延迟可能是糖尿病的相同全身缺陷的表现，包括通过巨噬细胞表型改变损伤的细胞和分子信号的损害。糖尿病所致的高脂血症可能通过巨噬细胞功能的改变和随后创面细胞因子的失调而干扰创伤的正常细胞和分子信号。结果：动物模型和人类的初步数据表明，高血糖与血清低密度脂蛋白和三甘油的升高相结合，导致晚期糖基化终产物(AGEs)的形成，从而可能改变巨噬细胞的表型。这可能是巨噬细胞细胞因子产生的失调以及炎性组织破坏和牙槽骨丢失增加的原因。应用：未来的研究将在全身性创伤愈合缺陷的背景下考虑糖尿病帕金森病，在面对持续的牙龈病理性损伤(菌斑)时表现为帕金森病，或者在身体其他部位周期性创伤性损伤的情况下延迟皮肤伤口愈合。这些类型的研究将提供有关糖尿病患者缺陷组织修复的信息，这些信息将对理解帕金森病和延迟皮肤愈合以及适当和特定治疗的应用具有临床意义。
BACKGROUND: Diabetes mellitus is a major health problem in the United States affecting approximately 13 million people. The five ‘classic’ complications which have historically been associated with the condition are microangiopathy, neuropathy, nephropathy, microvascu‐lar disease, and delayed wound healing. Recently, per‐iodontal disease (PD) has been declared the ‘sixth’ major complication of diabetes as diabetics demonstrate an increased incidence and severity of PD. The cellular and molecular basis for diabetic PD is unknown.HYPOTHESIS: Recent evidence suggests that PD and delayed dermal wound healing may be manifestations of the same general systemic deficit in diabetes involving impairment of the cellular and molecular signal of wounding via alterations in macrophage phenotype. Diabetes‐induced hyperlipidemia may interfere with the normal cellular and molecular signal of wounding by alteration of macrophage function and subsequent dysregulation of cytokines at the wound site.RESULTS: Preliminary data in both animal models and humans suggests that hyperglycemia, in combination with elevations of serum low density lipoproteins and tri‐glycerides, leads to formation of advanced glycation end products (AGES) which may alter macrophage phenotype. This may be responsible for dysregulation of macrophage cytokine production and increased inflammatory tissue destruction and alveolar bone loss.IMPLICATIONS: Future investigations will consider diabetic PD in the context of a generalized systemic wound healing deficit that manifests as PD in the face of constant pathologic wounding of the gingiva (bacterial plaque) or delayed dermal wound healing in instances of periodic traumatic wounding to other parts of the body. These types of studies will provide information concerning defective tissue repair in diabetics that will have clinical relevance for the understanding of PD and delayed dermal healing as well as applications of appropriate and specific therapies.
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影响因子：
6.7
作者：
B. Safkan;J. Ainamo
通讯作者：
J. Ainamo
糖尿病和牙周病患者。
影响因子：
4.3
作者：
Kent A. Hove;Richard E. Stallard
通讯作者：
Richard E. Stallard
一种针对分化抗原的单克隆抗体，存在于成熟人巨噬细胞上，但单核细胞中不存在。
影响因子：
4.4
作者：
G. Zwadlo;E. Bröcker;D. B. V. Bassewitz;U. Feige;C. Sorg
通讯作者：
C. Sorg
DOI：
10.1056/nejm198805193182007
发表时间：
1988-05
期刊：
The New England journal of medicine
影响因子：
--
作者：
M. Brownlee;A. Cerami;H. Vlassara
通讯作者：
M. Brownlee;A. Cerami;H. Vlassara
脂肪酸摄入和库普弗细胞功能：鱼油改变类二十烷酸和单核因子的产生以刺激内毒素。
影响因子：
3.8
作者：
T. Billiar;P. Bankey;Svingen Ba;R. D. Curran;M. West;R. Holman;R. L. Simmons;F. Cerra
通讯作者：
F. Cerra