Arunachalam Lalitha Tanjore, Rao Suresh
Department of Periodontics, Thai Moogambigai Dental College, Golden George Nagar, Chennai, India.
Indian J Dent Res. 2013 Mar-Apr;24(2):255-60. doi: 10.4103/0970-9290.116695.
Drug-induced gingival overgrowth (DIGO) is one of the unwanted side effects of amlodipine therapy, but the pathogenesis still remains unclear. Apoptosis, which plays a ubiquitous role in tissue homeostasis, including gingiva, may be involved in the development of gingival enlargement.
(i) To study the distribution of Bcl-2 in healthy and overgrown gingival tissues. (ii) To compare and correlate the Bcl-2 expression in gingival samples from subjects on amlodipine therapy to the findings in healthy controls.
A total of 25 subjects were recruited for the study - 15 hypertensive patients and 10 systemically healthy subjects. Both the groups were analyzed for Bcl-2 expression using immunohistochemistry.
Few of the control specimens showed weak positivity to Bcl-2 antibody, with the distribution limited to the basal cell layers alone, whereas 10 hyperplastic specimens expressed Bcl-2 and, unlike the control group, the distribution pattern was seen in both basal and suprabasal layers.
The results indicate that the pathogenesis of amlodipine-induced gingival overgrowth might involve inhibition of apoptosis, especially with morphogenesis of hyperplastic gingival epithelia.
药物性牙龈增生(DIGO)是氨氯地平治疗的不良副作用之一,但其发病机制仍不清楚。凋亡在包括牙龈在内的组织稳态中普遍发挥作用,可能参与牙龈增生的发生发展。
(i)研究Bcl-2在健康和增生牙龈组织中的分布。(ii)比较并关联接受氨氯地平治疗的受试者牙龈样本中Bcl-2的表达与健康对照的结果。
共招募25名受试者进行研究——15名高血压患者和10名全身健康受试者。两组均采用免疫组织化学分析Bcl-2表达。
少数对照标本对Bcl-2抗体呈弱阳性,分布仅限于基底细胞层,而10个增生标本表达Bcl-2,与对照组不同,在基底和基底上层均可见分布模式。
结果表明,氨氯地平诱导的牙龈增生的发病机制可能涉及凋亡抑制,尤其是增生性牙龈上皮的形态发生。