The highest values of sensitivity for the diagnosis of periodontitis were obtained for IL1beta (78.7%), followed by MMP8 (72.5%), IL6 and haemoglobin (72.0% for both molecules); the lowest sensitivity value was for MMP9 (70.3%).
When comparing genotype/allele frequencies in periodontitis versus healthy and periodontitis versus gingivitis scenarios, the number of positive associations (2-4) and the degree of association (p and odds ratio values) were significantly increased by the new approach proposed (periodontitis versus gingivitis), suggesting the association of IL1B-3954, TNFA-308, IL10-592 and TLR4-299 with periodontitis risk.
Indicators of inflammation may be important clinical determinants of future periodontal disease progression, but the IL-1 genotype was not a risk indictor for early (slight) periodontitis as defined in this subject population.
One previous meta-analysis has been published on this topic and supported an association between IL-1 genes and periodontitis, but considerable doubt remains about the patient populations in which the association may be of clinical relevance.
Are selected IL-1 polymorphisms and selected subgingival microorganisms significantly associated to periodontitis in type 2 diabetes patients? a clinical study.
Also, we found three negative associated haplotypes with PE: IL-1α + 4845 G/IL-1β -511 A, IL-1β + 3954 C/IL-1β -511 A and interestingly IL-1α -889 C/IL-1β -511 A also with a positive association with RA.
Subjects bearing at least one copy of the variant allele 2 at positions IL-1A -889 and IL-1B +3954 (genotype positive) had an enhanced smoking-associated periodontitis risk as compared to their IL-1 genotype-negative counterparts.
Polymorphisms in the interleukin-1 (IL1) gene have been suggested to influence transcription of IL1A (interleukin-1alpha) and IL1B (interleukin-1beta) and thereby the pathophysiology of periodontitis.
Interleukin-1 beta (IL-1 beta) is a potent regulator of osteoprogenitor cells and fibroblasts, and is believed to be responsible for the bone loss and connective tissue breakdown that occurs in periodontitis.
This may suggest that among subjects undergoing SPT, a lower bacterial load is required in IL-1 gene-positive subjects to develop the same level of periodontitis as in IL-1 gene-negative subjects.
The similarity in systemic inflammation between patients and controls suggests that the increased release/generation of IL-1beta and oxygen radicals from peripheral leukocytes in periodontitis patients is of a constitutional nature and of pathogenic relevance.
In response to pulp exposure, the bone loss and level of MIF mRNA increased in the periradicular periodontitis, which peaked at 14 d, in conjunction with the upregulated expressions of mRNAs for RANKL, proinflammatory cytokines (TNF-α, IL-6, and IL-1β), chemokines (MCP-1 and SDF-1), and MIF's cognate receptors CXCR4 and CD74.
A total of 106 patients hospitalized with ACS or angina were compared to a group of 1,959 individuals tested for susceptibility to periodontitis by profiling the IL-1 gene.
Moreover, cranberry PACs reduced caspase-1 activation in LtxA-treated macrophages and consequently decreased the release of both IL-1β and IL-18, which are known as damage-associated molecular patterns (DAMPs) and contribute to the progression of periodontitis by increasing cell migration and osteoclastogenesis.
Salivary IL-1β and MMP-8 might be useful for diagnosing periodontitis and monitoring the recovery of periodontitis following nonsurgical periodontal therapy.