Sexual dimorphism in periapical inflammation and bone loss from mitogen-activated protein kinase phosphatase-1 deficient mice.
BACKGROUND
Mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) has been shown to be a key negative regulator of the MAPK pathways of the innate immune system. The impact of MKP-1 in an endodontic model has yet to be studied. Thus, the purpose of this study was to determine the role of MKP-1 in a bacterial-driven model of pathologic endodontic bone loss.


METHODS
Pulps were exposed in both lower first molars of 10-week-old mkp-1(+/+) and mkp-1(-/-) mice and left open to the oral environment for either 3 or 8 weeks. At death, mandibles were harvested and scanned by micro-computed tomography (μCT) to determine periapical bone loss. Histopathologic scoring was then performed on the samples to determine the amount of inflammatory infiltrate within the periapical microenvironment.


RESULTS
Significant bone loss and inflammatory infiltrate were found in all experimental groups when compared with control. No statistical difference was found between mkp-1(+/+) and mkp-1(-/-) at either time point with respect to bone loss or inflammatory infiltrate. At 8 weeks, male mkp-1(-/-) mice were found to have significantly more bone loss and inflammatory infiltrate when compared with female mkp-1(-/-) mice. There was also a significant correlation between an increase in bone loss and increase in inflammatory infiltrate.


CONCLUSIONS
A sexual dimorphism exists in the periapical inflammatory process, where male mkp-1(-/-) mice have more inflammation than female mkp-1(-/-) mice. The increase in inflammatory infiltrate correlates to more bone loss in the male mice.
Department of Oral Rehabilitation, Division of Endodontics, Medical University of South Carolina, 173 Ashley Ave., Charleston, SC 29425, USA.
Justin
J
McAbee
Qiyan
Q
Li
Hong
H
Yu
Keith L
KL
Kirkwood
D016301:Alveolar Bone Loss / Q000201:enzymology* / Q000382:microbiology; D000818:Animals; D003789:Dental Pulp Exposure / Q000382:microbiology; D054638:Dual Specificity Phosphatase 1 / Q000235:genetics / Q000502:physiology*; D005260:Female; D007091:Image Processing, Computer-Assisted; D007113:Immunity, Innate / Q000276:immunology; D007249:Inflammation; D020935:MAP Kinase Signaling System / Q000276:immunology; D008297:Male; D008336:Mandibular Diseases / Q000201:enzymology / Q000382:microbiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008963:Molar / Q000382:microbiology; D009504:Neutrophils / Q000473:pathology; D010485:Periapical Periodontitis / Q000201:enzymology* / Q000382:microbiology; D012727:Sex Characteristics; D013997:Time Factors; D055114:X-Ray Microtomography
D054638:Dual Specificity Phosphatase 1; C517020:Dusp1 protein, mouse