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2022, Vol. 26 ›› Issue (14): 2179-2183

Changes in programmed necrosis pathway in the occurrence and development of periapical periodontitis in a mouse model

Liu Jie, Wang Min   

  1. State Key Laboratory of Oral Disease Research, National Oral Disease Clinical Research Center, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan Province, China

  • Received:2021-01-21 Revised:2021-01-28 Accepted:2021-03-24 Online:2022-05-18 Published:2021-12-21

  • Contact: Wang Min, MD, Professor, State Key Laboratory of Oral Disease Research, National Oral Disease Clinical Research Center, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan Province, China

  • About author:Liu Jie, Master candidate, State Key Laboratory of Oral Disease Research, National Oral Disease Clinical Research Center, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan Province, China

  • Supported by:

    the National Natural Science Foundation of China, No. 82001060; Sichuan Province Regional Innovation Cooperation Project, No. 2020YFQ0008; the Sichuan Provincial Science and Technology Foundation, Nos. 2020YFS0174 and 2019YFS0359



Abstract: BACKGROUND: Programmed necrosis is related to many inflammatory diseases, but there are few studies on its relationship with oral diseases, and the research on its relationship with apical periodontitis has not been reported.
OBJECTIVE: To explore the changes of programmed necrosis pathway in apical periodontitis in a mouse model.
METHODS: Thirty 12-week-old male balb/c mice were randomly divided into control group and experimental group according to the random number table method. After 1 week of acclimatization, the experimental group underwent anesthesia to open the bilateral mandibular first molars. To establish a mouse model of periapical periodontitis, the pulp cavity was colonized with concentrated Fusobacterium nucleatum fluid, and sealed with temporary sealing cream. The control group only underwent anesthesia. After 7 days, the mouse mandibles were dissected, and bone resorption was analyzed by Micro-CT. qPCR was used to detect the expression of RIP3 and inflammatory factors, interleukin-1α, interleukin-1β and tumor necrosis factor-α mRNA; and western-blot and immunohistochemical analysis were used to analyze the expression of key molecules RIP3 and pMLKL. The study protocol was approved by the Experimental Animal Ethics Committee of West China School of Stomatology, Sichuan University, with the approval No. WCHSIRB-D-2020-423.

RESULTS AND CONCLUSION: Compared with the control group, the experimental group had more periapical bone absorption, and the periapical bone volume fraction and bone density decreased significantly (P < 0.01). Compared with the control group, the experimental group had higher mRNA expression of bone inflammatory factors, including interleukin-1α, interleukin-1β and tumor necrosis factor α, and protein expression of RIP3 and pMLKL in the programmed necrosis pathway. The above results indicate that the occurrence and development of apical periodontitis may be related to the activation of programmed cell necrosis.

Key words:programmed necrosis, apical periodontitis, MLKL, RIP3, inflammation


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