In this study caries associates inversely with the formation of IAs, but not with aSAH. Caries is the most common disease globally affecting nearly 3.5 billion people worldwide . Despite the fact that caries is more prevalent in high-socioeconomic states , our study of high-socioeconomic population, did not associate caries to a greater risk of IA and aSAH. There are several explanations for the lack of association: first the nature of caries is a local infectious disease of the tooth structure with systemic responses only when the caries reaches the tooth pulp. Secondly, caries is most often treated with fillings before severe conditions, such as inflammation of tooth pulp or periapical abscesses occur. However these caries-related conditions remain a challenge to oral health care providers. Thirdly, caries does not predispose to bacteremia contrary to periodontal diseases of the gingival tissues.
The association studies of oral bacteria with vascular diseases, including sIA/aSAH concentrate mostly on periodontal bacteria. Regarding cariogenic bacteria, a Japanese study  linked specific cnm strain of Streptococcus mutans to sIA. This specific strain promotes platelet aggregation inhibition and matrix metalloproteinase-9 activation which can logically be linked with sIA formation and rupturing. Although in our study caries did not associate with sIA disease, the finding of Inenaga et al may be explained by the poor oral hygiene predisposing to a poorer periodontal status. Via inflamed periodontal tissues this specific S. mutans strain could disseminate to circulation and to IA walls. This explanation is, however, highly speculative.
Other dental infections as risk factors for IA formation and subsequent aSAH
Whereas caries does not appear to associate with IA and aSAH, gingivitis and periodontitis, however, have been shown to associate to both IAs and aSAH [8-10,22]. Similar association of periodontitis to IAs and aSAHs that we have previously reported in the KUH cohort , was also clear in this study with TaUH patient cohort with geographically matched healthy controls. Furthermore, previously a plethora of studies have associated periodontitis to cardiovascular diseases [14,20] and this further demonstrates the crucial role of gingival pocket health as the border between systemic circulation and oral cavity. The association between oral infections and vascular diseases could be explained by either (i) direct effect on local bacterial infection on systemic low grade inflammation response, (ii) bacteremia and subsequent distant local infections (such as endocarditis) or (iii) similar genetic background of the diseases. Periodontal pathogens correlate to diseases/medical states of which pathogenesis is strongly linked to collagen degradation caused by MMP activation in different sites of the human body [4,11,25], such as pre-term birth and low birthweight , cardiovascular diseases  and periodontitis . A single specific finding that further explains the association was introduced by Aarabi and colleaques in 2017. They described common genetic background of periodontal destructive and vascular destructive states . The involvement of shared genetic background of the diseases could also explain the associations: Some people are prone to both periodontal disease and cardiovascular diseases, and the bacteria invade the vascular wall if they are given the chance by genetic factors. Pathomechanisms of caries are not similar with these collagen degradative states seen in periodontal diseases.
Since periodontal diseases associate with sIA disease and increase the risk of aSAH in the long term, but other oral diseases, to our knowledge, do not, the effect and association might be explained by the nature of the disease itself rather than periodontal disease being only an “innocent co-variant” reflecting for example poor socioeconomic status to which many IA risk factors associate to. A prior study on the bacterial DNA present in IA wall tissue have not been able to discriminate whether periodontal or cariogenic pathogens associate with IAs, but rather DNA of pathogens related to both groups are found in the IA wall . This discrepancy between the bacterial DNA findings and the clinical finding that nevertheless only periodontal disease associates with IA formation or rupture could be explained by the bleeding wound surface in inflamed gingival pocket forming a gateway for oral bacteria to enter the systemic circulation, and eventually the IA wall. Further studies on this hypothesis are warranted.
Limitations of the study
Our study has some limitations due to its design. First, we could not recruit all IA and aSAH patients to the study due to patients denial to participate or due to tight schedule of the examining dentists. The use of healthcare registry data has always a source of bias. Also, our comparison between KUH and TaUH patients to participants of Health 2000 –survey has its limits, since there is a 15-16 year gap between oral examinations. Also, single person performing the oral examination (JH in KUH and MP in TaUH) could lead to over- or underestimations of oral conditions.