Association of IL-10 and TNF-α Polymorphisms with Dental Peri-Implant Disease Risk: A Meta-Analysis, Meta-Regression, and Trial Sequential Analysis

Abstract

Genetic susceptibility has been reported to be an important risk factor for peri-implant disease (PID). The aim of this meta-analysis was to assess the association between TNF-α and IL-10 polymorphisms and PID susceptibility. The Web of Science, Cochrane Library, Scopus, and PubMed/Medline databases were searched for studies published until 12 April 2021. RevMan 5.3, CMA 2.0, SPSS 22.0, and trial sequential analysis software were used. Twelve studies were included in our analysis. The pooled ORs for the association of TNF-α (−308 G > A), IL-10 (−1082 A > G), IL-10 (−819 C > T), and IL-10 (−592 A > C) polymorphisms were 1.12, 0.93, 1.35, and 0.77 for allelic; 1.42, 0.95, 3.41, and 0.34 for homozygous; 1.19, 1.88, 1.23, and 0.49 for heterozygous, 1.53, 1.12, 1.41, and 0.39 for recessive; and 1.16, 1.87, 2.65, and 0.75 for dominant models, respectively, with all the estimates being insignificant. The results showed an association between TNF-α (−308 G > A) polymorphism and the risk of PID in patients of Asian ethnicity (OR = 1.59; p = 0.03). The present meta-analysis illustrated that TNF-α (−308 G > A), IL-10 (−1082 A > G), IL-10 (−819 C > T), and IL-10 (−592 A > C) polymorphisms were not associated with the risk of PID, whereas TNF-α (−308 G > A) polymorphism was associated with an elevated risk of PID in Asian patients.

Serum TNF-α level and probing depth as a combined indicator for peri-implant disease

“…Several studies have shown that IL-6, IL-10, TNF-α, and TGF-β1 are closely related to the occurrence and development of PID ( 21 ). IL-6 is a pro-inflammatory factor that promotes the growth and differentiation of osteoclast precursors and alveolar bone resorption ( 22 ), and IL-10 is an important regulator of the pro-inflammatory process, downregulating the synthesis of Th1 pro-inflammatory cytokines and preventing the occurrence of excessive inflammation by acting on macrophages ( 23 ). TNF-α can be produced and released by a variety of cells in the body, with monocyte/macrophages being its main source ( 23 ), and it is one of the key cytokines regulating alveolar bone reconstruction ( 24 ).…”

Association between Interleukin-1 Polymorphisms and Susceptibility to Dental Peri-Implant Disease: A Meta-Analysis

“…In this view, meta-analyses [6][7][8][9][10], reviews [11], and original articles [12,13] demonstrated the role of several polymorphisms in PIDs. Proinflammatory cytokines, such as interleukins (ILs), are important biochemical mediators to control the host response to inflammation and to also stimulate the production and secretion of prostaglandins.…”

“…Peri-implantitis can lead to bone loss and finally implant failure [4,5]. Peri-implantitis, marginal bone loss, and implant failure are three outcomes associated with peri-implant diseases (PIDs) [6,7]. PID is a collective term for reversible peri-implant mucositis and irreversible peri-implantitis [8].…”

“…A thorough literature search identified five systematic reviews [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] and three metaanalyses [10][11][12][13][14][15][16][17][18][19][20][21][22] focusing on the associations between IL−1 polymorphisms and PIDs. Among these meta-analyses, one meta-analysis [10] included the highest number of articles (13 articles) and reported an association between the occurrence of IL−1A (−889), IL−1B (−511), and IL−1B (+3954) polymorphisms in patients with PIDs.…”

Histological and Immunohistochemical Analysis of Peri-Implant Soft and Hard Tissues in Patients with Peri-Implantitis

“…Peri-implantitis (PI) is characterized by the inflammation and destruction of peri-implant bone tissue, leading to implant failure and loss [ 1 ]. Currently, the research mainly focuses on inflammatory mediators, cells, or molecules related to the PI etiopathogenesis, which could serve as molecular markers useful in the early diagnosis, prognosis, and treatment of the disease [ 2 , 3 , 4 , 5 , 6 ].…”