Chronic stress may modulate periodontal disease: a study in rats.
BACKGROUND
The present study aimed to evaluate whether chronic stress (CS) affects ligature-induced periodontal disease and to investigate the impact of CS on the mRNA levels of interleukin (IL)-1beta, -1 receptor antagonist, -6, and -10, interferon-gamma (IFN-gamma), receptor activator of nuclear factor-kappa B ligand (RANKL), and osteoprotegerin in the gingival tissues of rats.


METHODS
Sixty male Wistar rats were assigned randomly to three groups: G1 (control; non-ligated sites), G2 (periodontal disease), and G3 (periodontal disease associated with restraint stress for 12 hours/day for the entire study). After 30 days, all animals were sacrificed by decapitation. Blood samples were taken, and the concentrations of corticosterone and catecholamines were measured as biomarkers of CS. Marginal tissues around ligated and non-ligated teeth were harvested, and gene expression was assessed by quantitative polymerase chain reaction. Moreover, the area of bone loss (ABL) was determined histometrically.


RESULTS
Data analysis showed that CS increased serum levels of stress biomarkers (P <0.05), ligature placement resulted in a significant ABL compared to non-ligated sites, CS significantly increased the amount of ABL in inflamed sites (P <0.001), and CS significantly increased mRNA levels of proinflammatory (IL-1beta and -6 and IFN-gamma) and anti-inflammatory (IL-10) cytokines and proresorptive factor (RANKL) in ligated sites (P <0.05).


CONCLUSIONS
CS significantly increased bone loss resulting from ligature-induced periodontitis by a local increase in proinflammatory and proresorptive factors.
Peruzzo
Daiane C
DC
School of Dentistry at Piracicaba, State University of Campinas, Piracicaba, SP, Brazil.
Benatti
Bruno B
BB
Antunes
Isabela B
IB
Andersen
Monica L
ML
Sallum
Enilson A
EA
Casati
Márcio Z
MZ
Nociti
Francisco H
FH
Nogueira-Filho
Getúlio R
GR
D016301:Alveolar Bone Loss / Q000276:immunology / Q000503:physiopathology; D000818:Animals; D015415:Biomarkers / Q000097:blood; D002395:Catecholamines / Q000097:blood; D002908:Chronic Disease; D003345:Corticosterone / Q000097:blood; D005881:Gingiva / Q000473:pathology; D018836:Inflammation Mediators / Q000032:analysis; D007371:Interferon-gamma / Q000032:analysis; D053590:Interleukin 1 Receptor Antagonist Protein / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D053244:Osteoprotegerin / Q000032:analysis; D010518:Periodontitis / Q000276:immunology / Q000503:physiopathology*; D053245:RANK Ligand / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D013312:Stress, Physiological / Q000097:blood / Q000276:immunology / Q000503:physiopathology*
D015415:Biomarkers; D002395:Catecholamines; D018836:Inflammation Mediators; D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta; D015850:Interleukin-6; D053244:Osteoprotegerin; D053245:RANK Ligand; D012333:RNA, Messenger; D017472:Receptors, Interleukin-1; D016753:Interleukin-10; D007371:Interferon-gamma; D003345:Corticosterone