Myeloid derived suppressor cell: A new player in periodontal disease?
Periodontal disease can be initiated by a shift from a symbiotic to a dysbiotic microbial community. An increase in the recruitment of leukocytes and production of inflammatory cytokines, chemokines and oxidative stress are generated by this shift. In periodontitis, an exacerbated, poorly specific and effective inflammatory response is mounted. Moreover, failure in the inflammation resolving mechanism leads to establishment of a chronic inflammatory process, resulting in the progressive destruction of bone and soft tissue. In different diseases presenting chronic inflammation some important players of immune response are defectives. Thus, an immunosuppressive environment could be induced during chronic inflammation. Myeloid derived suppressor cells (MDSC), a heterogenic group of immature myeloid cells with potent immune suppressive activity, are increased in several acute and chronic inflammatory diseases. Dysbiosis-mediated inflammation can induce increased frequency of MDSC. In addition, mediators generated in diverse inflammatory diseases have demonstrated to promote expansion, activation and recruitment of MDSC, similar mediators have been described in periodontal disease. MDSC promote generation of nitric oxide (NO) and reactive oxygen species (ROS). Furthermore, MDSC can differentiate in functional osteoclasts. We hypothesize that MDSC are generated during periodontal disease. Review of literature evaluating this hypothesis and possible implications are assed in this work. It encourages the study of MDSC in this common disease.
Facultad de Odontología, Universidad Autónoma de Baja California, Mexicali, BC, Mexico.
Omar
O
Valero-Monroy
Facultad de Odontología, Universidad Autónoma de Baja California, Mexicali, BC, Mexico.
Gabriel
G
Garcia-Cervantes
Facultad de Odontología, Universidad Autónoma de Baja California, Mexicali, BC, Mexico.
Luis F
LF
Marquez-Corrales
Unidad de Ciencias de la Salud, Facultad de Medicina, Universidad Autónoma de Baja California, Mexicali, BC, Mexico.
Ana G
AG
Leija-Montoya
Área de Investigación Clínica, Unidad de Innovación Clínica y Epidemiológica de la Secretaría de Salud del Estado de Guerrero, Acapulco, Gro, Mexico.
Jorge
J
Sandoval-Basilio
Unidad de Ciencias de la Salud, Facultad de Medicina, Universidad Autónoma de Baja California, Mexicali, BC, Mexico.
Gustavo
G
Martinez-Coronilla
Facultad de Odontología, Universidad Autónoma de Baja California, Mexicali, BC, Mexico.
Mario A
MA
Isiordia-Espinoza
Facultad de Odontología, Universidad Autónoma de Baja California, Mexicali, BC, Mexico; Unidad de Ciencias de la Salud, Facultad de Odontología, Universidad Autónoma de Baja California, Mexicali, BC, Mexico. Electronic address: nserafin@uabc.edu.mx.
Nicolas
N
Serafin-Higuera
D018450:Disease Progression; D015536:Down-Regulation; D006801:Humans; D007107:Immune System; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007249:Inflammation; D059013:Microbial Consortia; D008962:Models, Theoretical; D000072737:Myeloid-Derived Suppressor Cells / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D010010:Osteoclasts / Q000378:metabolism; D018384:Oxidative Stress; D010510:Periodontal Diseases / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013234:Stem Cells / Q000166:cytology; D014070:Tooth / Q000503:physiopathology
D007166:Immunosuppressive Agents; D017382:Reactive Oxygen Species; D009569:Nitric Oxide