Cys–X–Cys ligand 9 might be an immunological factor in the pathogenesis of oral submucous fibrosis and its concomitant oral lichenoid lesion

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• 作者：Ning Li (1)
  Qiong Hu (2)
  Canhua Jiang (1)
  Feng Guo (1)
  Krishna Munnee (3)
  Xinchun Jian (1)
  Yanjia Hu (1)
  Zhangui Tang (1)
  
• 关键词：Immunological reaction ; CXCL9 ; Oral submucous fibrosis ; Oral lichenoid lesion ; Betel quid
• 刊名：Clinical Oral Investigations
• 出版年：2013
• 出版时间：May 2013
• 年：2013
• 卷：17
• 期：4
• 页码：1251-1258
• 全文大小：495 KB
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• 作者单位：Ning Li (1)
  Qiong Hu (2)
  Canhua Jiang (1)
  Feng Guo (1)
  Krishna Munnee (3)
  Xinchun Jian (1)
  Yanjia Hu (1)
  Zhangui Tang (1)
  
  1. Department of Oral and Maxillofacial Surgery, Xiangya Hospital, Central South University, Xiangya Road, Changsha, People’s Republic of China
  2. Department of Pain Management, The Second People’s Hospital, Furong Road, Changsha, People’s Republic of China
  3. Department of Plastic Surgery, Victoria Hospital, Candos, Mauritius
  
• ISSN：1436-3771

文摘

Objectives Oral submucous fibrosis (OSF) is a chronic oral precancerous disease primarily caused by betel quid chewing. Some OSF patients are concomitant with oral lichenoid lesion (OLL), a white-streak lesion with a higher risk for cancerization, in OSF mucosa. Immunological reaction has been considered as one of their common pathogenic mechanisms. Cys–X–Cys ligand 9 (CXCL9) is an important factor to recruit effector neutrophils and lymphocytes in immunological reactions. However, the expression levels of CXCL9 in OSF and OLL remain unclear. Materials and methods We investigated the expression levels of CXCL9 in 10 normal buccal mucosa (NBM) samples and 56 OSF concomitant with OLL patients, and evaluated the possible mechanism of CXCL9 on their pathogenesis. Results Our results showed NBM demonstrated negative CXCL9 expression. OSF stained positive CXCL9 mainly in the cytoplasm of inflammatory cells and endothelial cells throughout the superficial layer of connective tissue, while its concomitant OLL showed much stronger CXCL9 in all mononuclear cells of subepithelial inflammatory infiltration (p--.0006). There was an upregulated trend of CXCL9 expression from NBM to OSF to OLL. However, no significant association between CXCL9 expression and clinicopathologic parameters of patients was found. Conclusions In conclusion, CXCL9 was found for the first time to contribute to the immunological pathogenesis for both OSF and its concomitant OLL, indicating a continuously enhanced intensity of immunoreactivity in their pathogenic process. Clinical relevance CXCL9 might be a useful tool to monitor the phase and disease severity of OSF and OLL, and a potential target for further clinical therapy for both lesions.