The present study is a cross sectional study which estimated the levels of salivary interleukin-1β and sclerostin among ABO blood groups in patients with Stage III Grade A periodontitis.
Despite the fact that bacteria are the primary cause of periodontal disease, there is substantial evidence that host variables including genetic susceptibility can affect each person's clinical presentation, disease distribution and extent of destruction. Since it was discovered that antibodies and antigens are inherited in the early 1900s, associations between blood type and disease has been researched.[14] There has been debate on how ABO blood types affect the likelihood of getting oral diseases and a small group of researchers did not detect the increased risk that some authors claimed existed between ABO blood types and the development of oral diseases.[15] We will be able to identify those who are more at risk ,aid those who are vulnerable to the disease and stop the disease's progression by establishing a link between the ABO blood types and molecular markers of periodontal disease.
Saliva is a biological fluid with a wide range of applications. It is simple to collect non-invasively and the results of its examination complement clinical and histological findings in the diagnosis of a variety of disorders.[16] Wilton et al. reported one of the earliest investigations using saliva marker analysis for periodontitis. Till date the results of this 1st study still holds true which states that saliva may be used as a source of markers for disease activity or response to therapy rather than as a diagnostic tool. By associating the impacts of treatments on molecular and cellular pathways, the assessment of these molecular markers can assist in explaining the outcomes of clinical studies. It is also understood that these molecular markers have a role in controlling the immune response in periodontal diseases.[17] According to Ebersole et al., the salivary markers IL-1, IL-6, MMP-8, and MIP-1 alpha can be used to distinguish between gingivitis,periodontitis and healthy periodotium .[18]
IL-1β is a highly potent proinflammatory cytokine that has been discovered to be elevated in diseased state. It mediates in a wide range of immune reactions, including innate and adaptive immunity. A study by Ji Youn Kim et al concluded that IL-1β was a confirmed biomarker with a sensitivity of 88.24% and specificity of 62.5%.[19] The results of the present study suggests that there is a significant difference in the salivary levels of IL-1β among the healthy subjects and subjects with Stage III Grade A periodontitis, it being higher in the periodontitis group. IL-1β has been strongly influenced by the degree of periodontal tissue destruction and inflammation. The result is in accordance with a study conducted by Rachna et al which indicated a higher IL-1β levels in patients with chronic periodontitis than healthy controls.[20] In the present study the mean values of IL-1β was significantly less in blood type AB. It is possible that genetic variations in immune cell maturation and antigen presentation increase a person's vulnerability to dieases.[21] Contrary to this study, a study by Basima et al conducted on subjects with chronic periodontitis in Baghdad that suggested that serum IL-1β showed a statistically significant association with blood group B and but no significant association with blood group AB was seen due to the lack of sufficient subjects.[22] The ABO blood types are well recognised to show racial differences in their proportions.
Sclerostin, a protein that has been shown to be a powerful inhibitor of bone formation, decreases the viability of osteoblasts and osteocytes, which affects bone turnover and bone metabolism. It is known as a marker of mature osteocytes. Sclerostin's role in the progression of periodontitis has attracted more attention in recent years. Researchers have discovered that sclerostin production can be induced by inflammation.[23] The results of the present study suggests that there is a significant difference in salivary levels of sclerostin among the healthy subjects and subjects with Stage III Grade A periodontitis and no statistically significant difference in SOST levels was found among the blood groups. The other studies associating SOST and periodontitis has mostly determined GCF SOST levels. A study by Zeinab et al suggested that the in comparison to healthy controls, the group with chronic periodontitis had a considerably greater concentration of sclerostin in GCF.[24] Umut Balli found a strong positive correlation between GCF SOST levels and CAL and GI.[25] In majority of the studies, the SOST gene's discovery was linked to the phenotype of chronic periodontitis and bone resorption.[24]
In this study the mean scores of all the clinical parameters, BI, PI, GI, PD and CAL was higher in G2 than G1 irrespective of the blood groups. In this study equal number of subjects were selected as per the inclusion criteria for each group-44 healthy subjects and 44 subjects with Stage III Grade A periodontitis. They were further divided as per the 4 blood groups and 11 subjects were included in each blood group. As the same number of subjects were included in the blood groups and the same stage of disease was considered no statistically significant difference was seen with respect to the prevalence of disease based on the clinical parameters among the blood groups. Previous studies conducted distributed the subjects with periodontitis as per the highest frequency of blood groups. Studies by Koregal et al and Demir et al showed that periodontitis was more common in blood groups O while Al Ghamadi et al found blood group B to be at a greater risk for developing periodontitis.[5, 26, 27]A study by Vivek et al found that the propensity was least among AB blood groups.[28]
In this study males were more predominant. Except for A blood group in G1 which had more females, all other blood groups in both G1 and G2 showed male predominance. This study's results were in agreement with a research by Shaiu et al that found males to have a higher probability than women in developing destructive periodontal disease. This increase in risk for periodontitis could be due to a higher probability of males exhibiting more, sex differences in oral health-related behaviour and environmental factors. According to the gene-based model, the greater immunologic advantage of females would be related to cellular processes that depend on genes on the X chromosome or sex-specific variations in how autosomal gene content is regulated. Recent research offers a novel paradigm of disease vulnerability by suggesting that natural variation within the autosomal genomes impacts physiologic features, such as immune function differently in males and females. However, further sex-matched research are needed for conclusive conclusions regarding gender.[29]
To the best of my knowledge no other study till date has established an association between IL-1β and SOST in patients with Stage III Grade A periodontitis. Previously researchers such as Aravind et al conducted epidemiological studies in which subjects with periodontitis were divided as per the highest frequency of blood groups to establish a relationship between the blood groups and periodontitis.[30] In our study we divided the subject’s equally among the blood groups and estimated the levels of biomarkers to determine the blood group with the highest risk for periodontal disease. This is also the first study where levels of SOST has been determined in saliva. The previous studies conducted by researchers such as Chatzopoulos GS have determined the levels of SOST in GCF.[31]
One limitation of our study was that the clinical parameters were recorded and the salivary IL-1β and SOST levels were estimated only at baseline before the subjects underwent treatment. Measurements after treatment may facilitate better evaluations. Also different levels of disease severity needs to be assessed. It is common knowledge that the distribution of ABO blood types varies depending on race or ethnicity. It is also well known that the distribution of periodontal diseases varies proportionally by race. Therefore, more research in other racial groups is necessary. Due to the possibility that the small number of patients in the current study contributed to the lack of statistical significance regarding SOST among the blood types, longer-term studies with a larger sample size are also required.
Within the constraints of this study, it is reasonable to draw the conclusion that there is a relationship between ABO blood groups and periodontal disease markers like IL-1β and that blood types can be used as a genetic host factor to assess an individual's susceptibility to the disease. The evidence also points to salivary SOST as a possible indicator of periodontal disease. To establish a more thorough analysis of the impact of ABO groups on periodontal diseases, further multicentric, prospective, longitudinal and interventional studies in different races with varying levels of disease severity must be carried out.