Periodontitis and p38 mitogen activated protein kinase pathway: research and development

doi:10.3969/j.issn.2095-4344.2016.51.022

Abstract

Abstract:

BACKGROUND: A series of inflammatory signal pathways are activated accompanied by increasing expressions of inflammatory factors after periodontal tissues being stimulated by exogenous substances like bacterium. Inflammation is closely related to periodontal tissue repair and regeneration.
OBJECTIVE: To illustrate the correlation of immune response of periodontitis and periodontitis-related inflammatory cytokines to p38 mitogen activated protein kinase (p38MAPK) pathway, and to provide a new idea and method for the treatment of periodontitis in the future.
METHODS: The related literatures of periodontitis and p38MAPK pathway published from January 1990 to January 2016 were retrieved from the databases of CBM, CNKI, SWIC and PubMed. The research and progress of periodontal tissue repair and regeneration after periodontitis were analyzed.
RESULTS AND CONCLUSION: Totally 36 literatures were enrolled finally. Inflammation-regulated and inflammation-associated signaling pathways as well as subsequent expression of inflammatory mediators can partly control the excessive disease-induced inflammation and immune responses of the host, among which p38MAPK signaling pathway may be involved in the occurrence and development of periodontitis. More studies, however, are needed to validate these findings. The regulation of p38MAPK signaling pathway is still of great significance in the treatment of periodontal disease, and we hope to provide a new insight and basis for clinical diagnosis and treatment of periodontitis.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Tissue Engineering, Periodontitis, Inflammation, Immunity

CLC Number:

R318

Tang Ya-ping, Liu Qi, Guo Cheng-wei, Xie Rui-di . Periodontitis and p38 mitogen activated protein kinase pathway: research and development[J]. Chinese Journal of Tissue Engineering Research, 2016, 20(51): 7746-7752.

Figures/Tables 1

References

[1] Gemmell E, Marshall RI, Seymour GJ. Cytokines and prostaglandins in immune homeostasis andtissue destruction in periodontal disease. Periodontol. 1997; 14:112-143.

[2] Trowbridge HO, Emling RC. Inflammation. A review of the process. Implant Dent. 1997;6(3):238.

[3] Soares GMS, Figueiredo LC, Faveri M, et al. Mechanisms of action of systemic antibiotics used in periodontal treatment and mechanisms of bacterial resistance to these drugs. J Appl Oral Sci. 2012; 20(3):295-309.

[4] Chen FM, Sun HH, Lu H, et al. Stem cell-delivery therapeutics for periodontal tissue regeneration. Biomaterials. 2012;33(27):6320-6344.

[5] Górska R, Gregorek H, Kowalski J, et al. Relationship between clinical parameters and cytokine profiles in inflamed gingival tissue and serum samples from patients with chronic periodontitis. J Clin Periodontol. 2003;30(12):1046-1052.

[6] Havemose-Poulsen A, Sørensen LK, Stoltze K, et al. Cytokine profiles in peripheral blood and whole blood cell cultures associated with aggressive periodontitis, juvenile idiopathic arthritis, and rheumatoid arthritis. J Clin Periodontol. 2005;76(12):2276-2285.

[7] 孟焕新.牙周病学[M].3版.北京:人民卫生出版社,2000.

[8] Graves DT, Cochran D. The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction. J Periodontol. 2003;74(3):391-401.

[9] Rimondi E, Zweyer M, Ricci E, et al. Receptor activator of nuclear factor kappa B ligand (RANKL) modulates the expression of genes involved in apoptosis and cell cycle in human osteoclasts. Anat Rec (Hoboken). 2007;290(7):838-845.

[10] Schett G, Middleton S, Bolon B, et al. Additive bone-protective effects of anabolic treatment when used in conjunction with RANKL and tumor necrosis factor inhibition in two rat arthritis models. Arthritis Rheum. 2005;52(5):1604-1611.

[11] Yasuda H, Shima N, Nakagawa N, et al. Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL. Proc Natl Acad Sci U S A. 1998;95(7):3597-3602.

[12] 刘琪,Bartold M.慢性牙周炎中核因子κB受体活化子,护骨素和肿瘤坏死因子-α的蛋白表达[J].口腔医学,2004, 24(6):347-349.

[13] Liang L, Yu J, Wang Y, et al. Estrogen regulates expression of osteoprotegerin and RANKL in human periodontal ligament cells through estrogen receptor beta. J Periodontol. 2008;79(9):1745-1751.

[14] Nick JA, Young SK, Arndt PG, et al. Selective suppression of neutrophil accumulation in ongoing pulmonary inflammation by systemic inhibition of p38 mitogen-activated protein kinase. J Immunol. 2002; 169(9):5260-5269.

[15] Kim EK, Choi EJ. Compromised MAPK signaling in human diseases: an update. Arch Toxicol. 2015;89(6): 867-882.

[16] Arthur JSC, Ley SC. Mitogen-activated protein kinases in innate immunity. Nat Rev Immunol. 2013;13(9): 679-692.

[17] Li Z, Jiang Y, Ulevitch R J, et al. The primary structure of p38γ: a new member of p38 group of MAP kinases. Biochemical and biophysical research communications. 1996;228(2):334-340.

[18] Jiang Y, Gram H, Zhao M, et al. Characterization of the structure and function of the fourth member of p38 group mitogen-activated protein kinases, p38δ. J Biol Chem.1997;272(48):30122-30128.

[19] Wang Z, Harkins PC, Ulevitch RJ, et al. The structure of mitogen-activated protein kinase p38 at 2.1-Å resolution. Proc Natl Acad Sci U S A. 1997;94(6): 2327-2332.

[20] Han J, Lee J D, Bibbs L, et al. A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells. Science. 1994;265(5173):808-811.

[21] Park EJ, Park SW, Kim HJ, et al. Dehydrocostuslactone inhibits LPS-induced inflammation by p38MAPK-dependent induction of hemeoxygenase-1 in vitro and improves survival of mice in CLP-induced sepsis in vivo. Int immunopharmacol. 2014;22(2):332-340.

[22] Schieven GL. The biology of p38 kinase: a central role in inflammation. Curr Top Med Chem. 2005;5(10): 921-928.

[23] Hofbauer LC, Schoppet M. Clinical implications of the osteoprotegerin/RANKL/RANK system for bone and vascular diseases. JAMA. 2004;292:490-495.

[24] Matsumoto M, Sudo T, Saito T, et al. Involvement of p38 mitogen-activated protein kinase signaling pathway in osteoclastogenesis mediated by receptor activator of NF-kappa B ligand (RANKL). J Biol Chem. 2000;275(40):31155-31161.

[25] Lee HJ, Kang IK, Chung CP, et al. The subgingival microflora and gingival crevicular fluid cytokines in refractory periodontitis. J Clin Periodontol. 1995; 22(11):885-890.

[26] Graves DT, Delima AJ, Assuma R, et al. Interleukin-1 and tumor necrosis factor antagonists inhibit the progression of inflammatory cell infiltration toward alveolar bone in experimental periodontitis. J Periodontol. 1998;69(12):1419-1425.

[27] Patil C, Zhu X, Rossa C Jr, et al. p38 MAPK regulates IL-1beta induced IL-6 expression through mRNA stability in osteoblasts. Immunol Invest. 2004;33(2): 213-233.

[28] Holtmann H, Winzen R, Holland P, et al. Induction of interleukin-8 synthesis integrates effects on transcription and mRNA degradation from at least three different cytokine- or stress-activated signal transduction pathways. Mol Cell Biol. 1999;19(10): 6742-6753.

[29] Heidenreich O, Neininger A, Schratt G, et al. MAPKAP kinase 2 phosphorylates serum response factor in vitro and in vivo. J Biol Chem. 1999;274(20):14434-14443.

[30] Patil C, Rossa C Jr, Kirkwood KL, et al. Actinobacillus actinomycetemcomitans lipopolysaccharide induces interleukin-6 expression through multiple mitogen-activated protein kinase pathways in periodontal ligament fibroblasts. Oral Microbiol Immunol. 2006;21(6):392-398.

[31] Rossa C, Liu M, Patil C, et al. MKK3/6-p38 MAPK negatively regulates murine MMP-13 gene expression induced by IL-1β and TNF-α in immortalized periodontal ligament fibroblasts. Matrix Biol. 2005; 24(7): 478-488.

[32] 聂嘉,张博,顾斌,等.p38丝裂原活化蛋白激酶在炎症微环境作用下对牙周膜干细胞成骨分化的影响[J].中国医学科学院学报,2015,37(2):1-7.

[33] Lee HJ, Cho JW, Kim SC, et al. Roles of p38 and ERK MAP kinases in IL-8 expression in TNF-α-and dexamethasone-stimulated human periodontal ligament cells. Cytokine. 2006;35(1):67-76.

[34] Wu Y, Yang Y, Yang P, et al. The osteogenic differentiation of PDLSCs is mediated through MEK/ERK and p38 MAPK signalling under hypoxia. Arch Oral Biol. 2013;58(10):1357-1368.

[35] Li Q, Valerio MS, Kirkwood KL. MAPK usage in periodontal disease progression. J Signal Transduct. 2012;2012:308943.

[36] Rogers JE, Li F, Coatney DD, et al. A p38 mitogen-activated protein kinase inhibitor arrests active alveolar bone loss in a rat periodontitis model. J Periodontol. 2007;78(10):1992-1998