**4. Periodontitis and hypertension**

#### **4.1 Epidemiological associations between periodontitis and hypertension**

Hypertension is considered a major risk factor of CVD. Periodontitis has emerged as a new contributor to the complete cardiovascular risk profile of CVD.

The associative relationships between periodontitis and hypertension are important in the context of the high prevalence rates of both diseases that induce important medical and social burden. Besides the fact that periodontitis and hypertension share a group of common risk factors (older age, smoking, low socioeconomic and education status, genetics) an independent association between the two diseases has been reported.

The data provided by prospective and retrospective studies reported a higher prevalence of hypertension in patients with periodontal disease ranging from 7 to 77% as compared with patients without periodontitis with prevalence rates ranging from 4 to 70% [47]. Periodontitis patients had 4.5 mmHg higher systolic and 2.0 mmHg higher diastolic blood pressure than non-periodontitis patients [47]; the systolic component of the blood pressure seemed to be more influenced by periodontitis than the diastolic one [48].

Two meta-analyses provided information sustaining the association between periodontitis and hypertension [47, 49]. The heterogeneity of case definitions of both hypertension and periodontitis prevented the drawing of firm conclusions regarding this topic. The association between the two diseases is open to future analyses of data provided by clinical trials using uniform case definitions for periodontitis and hypertension.

The activity of periodontitis monitored through local inflammation index (bleeding on probing) seems also to play an important role in the complex interplay between periodontal disease and hypertension. Data from the Third US National Health and Nutrition Examination Survey (NHANES III) informed that local gingival inflammation (bleeding on probing) was significantly associated with increased systolic blood pressure (2.6 mmHg higher values compared with noninflamed situations) and increased risk of uncontrolled blood pressure after multivariate adjustments of a large make-up of influencing factors including systemic inflammatory diseases as well as behavioral and social factors [50]. Moreover, data from observational studies reported that even for patients on intensive antihypertensive treatment periodontitis was associated with an increased risk of uncontrolled hypertension [48].

The genetic background has been involved in the development of both periodontitis and hypertension at least partially by the modulation of immune-inflammatory reactions that sustain a proinflammatory milieu [48].

The high-salt diet is a common trigger for hypertension, but data has also shown to alter the microbiome and impair immune systems through salt-induced hyperglucocorticoidism [51, 52].

*Periodontitis and Heart Disease: Current Perspectives on the Associative Relationships… DOI: http://dx.doi.org/10.5772/intechopen.102669*

#### **4.2 Periodontitis and pregnancy hypertensive disorders**

It was proven that oral health among vulnerable populations, such as pregnant women is an important determinant regarding the pregnancy outcome. Numerous epidemiological studies have demonstrated an increased risk of adverse pregnancy outcome (APO), including preterm birth, low birthweight and pregnancy-induced hypertension or pre-eclampsia (PE) as well as gestational diabetes (GDM), related to periodontal disease [53]. Therefore, maintaining optimal maternal oral hygiene is regarded as a mandatory standard of care for perinatal medicine [54].

The reported prevalence of periodontitis, during the time period of pregnancy, varies between 10 and 74% and it is highly dependent on the economical level and health policies of each country [55].

Two pathogenic mechanisms described the potential effect of periodontal diseases on pregnancy outcomes. On the one hand, the periodontal bacteria could induce bacteremia and a seeding of the feto-placental unit. On the other hand, inflammatory mediators such as interleukin-1 (IL-1), IL-6, IL-8, tumor necrosis factor-α (TNF-α) or prostaglandin E2 (PGE2), secreted by the subgingival inflammatory site are carried to the feto-placental unit, where an inflammatory response will develop [53].

The influence of the gingival bacterial microbiome on APO is confirmed by the new data that revealed the presence of a unique bacterial load even of the placentar tissue. Gram-positive as well as Gram-negative intracellular bacteria were identified in the basal plate of the human placenta [56]. Moreover, due to metagenomic technology, it was shown that placental microbiome profiles are more related to the oral microbiome than other microbiomes in the human body, such as the gut, nares, skin and urogenital tract [57].

The feto-maternal unit is exposed to oral bacteria during bacteriemia episodes caused by daily oral activities (e.g., tooth brushing and flossing) and dental treatments (e.g., scaling and root planing). Katz et al. identified the presence of *Porphyromas gingivalis* antigens in placental tissues and suggested that the colonization of *Porphyromas gingivalis* in the placenta might contribute to the placental dysfunction, a specific obstetrical feature in severe cases of PE [58]. Moreover, the presence of *Porphyromas gingivalis* in the umbilical cord was highly associated with PE. Several meta-analyses found a risk at least twice higher to develop preeclampsia in women diagnosed with periodontitis [59, 60].

The relationship between hypertensive disorders (including both pregnancy preexisting hypertension and pregnancy-induced hypertension, also called preeclampsia) and periodontitis was mostly explained in relation to the systemic inflammatory response due to maternal infection. In severe cases of periodontitis, the inflammatory mediators (alarmins) and cytokines found in the gingival mucosa, including IL-1β, IL-6, TNF-α and PGE2, entered systemic circulation and affect the feto-placental unit and myometrium [53].

The adequate invasion of the extravillous trophoblast in the vascular layer of spiral uterine arteries will determine appropriate feto-maternal perfusion. In vitro models showed the local interaction between the placental tissue (human trophoblast cell lines) and periodontal pathogens, bacterial components, or inflammatory mediators. According to the data, the inflammatory milieu may suppress the media layer invasion process, leading to an important vascular remodeling. Eventually, that will trigger the development of pregnancy-induced hypertension or will aggravate the chronic vascular changes in pregnant women with preexisting hypertension. This will further cause placental insufficiency, the physiopathological final step to the development of fetal distress in utero [61].
