A systematic review and meta-analysis was conducted in an attempt to clarify whether IL-1 gene variants were associated with well-defined clinical phenotypes of CP in white patients.
Although the concentration of caspase-1 in saliva samples makes its determination useless for detection of periodontal disease and/or its severity, salivary levels of NLRP3, ASC, and IL-1β may act as strong/independent indicators of amount and extent of periodontal breakdown in both CP and AgP and could potentially be used for prevention and therapy of this group of diseases.
Comparing the efficiency of Er,Cr:YSGG laser and diode laser on human β-defensin-1 and IL-1β levels during the treatment of generalized aggressive periodontitis and chronic periodontitis.
Considering the effects of adjunctive aPDT as compared to SRP on clinical signs of CP in T2DM and smokers, no difference could be observed for all evaluated parameters (PD: Z=-0.81, P=0.41; CAL: Z=-0.19, P=0.84) except IL-1β (Z=4.57, P<0.001).
For IL1B polymorphism, two out of seven studies found a significant statistical association between EARR and CC genotype, whether for CP, there were eighth out of fifteen references describing a statistically significant associations with T allele.
Further analysis of gingival tissues by quantitative real-time PCR, however, indicates that despite a threefold increase in the expression of interleukin-1beta (IL-1beta) mRNA during CP, there is significant (30-fold) downregulation of TLR2 mRNA (P < 0.05, Student's t test).
GCF IL-1β levels at 6 weeks in FMF-CP group were significantly lower than the CP group (p < 0.05), and GCF IL-1ra levels were significantly decreased at 6 week in the FMF-CP group (p < 0.05).
However, other studies have reported conflicting findings, not only on the association between the composite IL-1 gene polymorphisms and CP, but also the link between IL-1 gene polymorphisms and aggressive periodontitis (AgP).
In the present study, TNF-alpha and IL-1 beta production by oral and peripheral blood polymorphonuclear leukocytes (PMN) was examined in 40 patients with adult periodontitis and 40 orally healthy matched controls.
In the study reported here, the frequency of IL-1beta genotypes including allele 2 of the IL-1beta+3953 restriction fragment length bi-allelic polymorphism was significantly increased in patients with advanced adult periodontitis compared to those with early and moderate disease.
LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis.
Multivariate logistic regression models demonstrated that patient age, former smoking history, and the IL-1 genotype were significantly associated with severity of adult periodontitis.
Our results provide evidence that polymorphisms in genes of the IL-1 family are associated with severe adult periodontitis in the absence of other risk factors tested in this patient population.
Patients with CP and uncontrolled T2D presented severe periodontal disease and inflammation (PPD, p = 0.0072; CAL, p = 0.0480; bone loss, p = 0.0088), higher levels of CASP1 mRNA expression (p = 0.0026), a stronger pattern of staining for NLRP3 and ASC proteins in the epithelium and connective tissues, and significantly higher production of IL-18 (p = 0.0063) and IL-1β (p = 0.0018) in comparison with healthy or CP subjects.
Polymorphisms in the interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) genes have been associated with an increased severity of chronic periodontitis.
Porphyromonas gingivalis (Pg), one of the main periopathogens, initiates an inflammatory cascade by host immune cells thereby increasing recruitment and activity of osteoclasts, the bone resorbing cells, through enhanced production of the crucial osteoclastogenic factor, RANK-L. Antibodies directed against some cytokines (IL-1β, IL-6 and TNF-α) failed to exhibit convincing therapeutic effect in CP.
Positive genotype heterozygous of allele 1 and 2 for IL-1β+3954 and IL-1α-889 did not represent in this study a major risk for chronic periodontitis (p=0.590).