**5. Risk-related dental procedures**

In 1935, Okell and Elliott detected positive blood cultures in more than half of patients undergoing dental manipulations, with a particularly high prevalence among those with deficient oral health. Since that time, the relationship between bacteraemia of oral origin and dental interventions constituted proof that endocardial infection could be precipitated by oral streptococci mobilised during dental manipulation [21].

Transient bacteraemia has been widely documented as a common finding during dental procedures, associated particularly with the manipulation of teeth and periodontal tissues. Non-surgical tooth extraction is the dental procedure that most frequently provokes bacteraemia of oral origin, with a detection rate of positive blood cultures of 58–100% (**Figure 1**).

**Figure 1.** Prevalence of oral bacteraemia after dental procedures (inferred from [11]).

From early studies, it was generally accepted that the incidence and magnitude of bacteraemia of oral origin during dental procedures was directly proportional to the degree of inflammation and infection in the mouth. However, more recent series have found no relationship between the number of caries or the presence of periapical lesions and increased risk of post-intervention bacteraemia. Similarly, it is also accepted that the grade of gingival and periodontal health does not affect the presence or intensity of bacteraemia during interventions, and an increase in the prevalence of bacteraemia has only been demonstrated after tooth extractions in the setting of an acute infectious condition.

**1.** Patients with any prosthetic valve, including a transcatheter valve, or those in whom any prosthetic material was

**b.** Any type of CHD repaired with a prosthetic material, whether placed surgically or by percutaneous techniques, up to 6 months after the procedure or lifelong if residual shunt or valvular regurgitation remains.

**Table 6.** Cardiac conditions associated with the highest risk of adverse outcomes of endocarditis according to the

In 1935, Okell and Elliott detected positive blood cultures in more than half of patients undergoing dental manipulations, with a particularly high prevalence among those with deficient oral health. Since that time, the relationship between bacteraemia of oral origin and dental interventions constituted proof that endocardial infection could be precipitated by oral

Transient bacteraemia has been widely documented as a common finding during dental procedures, associated particularly with the manipulation of teeth and periodontal tissues. Non-surgical tooth extraction is the dental procedure that most frequently provokes bacteraemia of oral origin, with a detection rate of positive blood cultures of 58–100% (**Figure 1**).

used for cardiac valve repair.

24 Contemporary Challenges in Endocarditis

**2.** Patients with a previous episode of infective endocarditis.

**3.** Patients with congenital heart disease (CHD):

**a.** Any type of cyanotic CHD.

European Society of Cardiology guideline [13].

**5. Risk-related dental procedures**

streptococci mobilised during dental manipulation [21].

**Figure 1.** Prevalence of oral bacteraemia after dental procedures (inferred from [11]).

Studies that have investigated the bacteriological spectrum of bacteraemia of oral origin show a wide variability in their results due to the different sampling and detection techniques employed. However, *Streptococcus* spp.—the bacterial species most frequently implicated in IE of oral origin—is detected in at least 30% of cases [22]. This inoculum of streptococci that reaches the bloodstream has intrinsic pathogenic potential to colonise susceptible endocardial tissue in highest-risk patients. Structurally, streptococci have surface proteins (adhesins) that have been shown experimentally to have high affinity for the extracellular matrix, making the microorganisms capable of easily colonising vegetations and medical devices that become coated with matrix proteins after implantation. After colonisation, the bacterial biofilm acts as a propitious environment to perpetuate infection. The resulting fibrin and platelet deposition over the biofilm contributes to organise an actual bacteria-release clot which is able to create the recurrent bacteraemias that characterise IE.

A number of experimental studies have been able to reproduce these pathological events in animal models, but it remains to be seen whether oral bacteraemia secondary to dental interventions could promote identical results in humans [23].

A prospective study recently performed on patients diagnosed with IE appears to indicate that the mouth is a potential portal of entry (POE) for IE. A sample of 318 patients diagnosed with IE was examined prospectively by different specialists selected according to the natural habitat or site of colonisation of the causal diagnosed microorganism. A potential oral POE was detected by a stomatologist in 68 cases (21%), of which only 12% were considered possibly related to previous professional manipulation. Interestingly, the highest percentage of patients (88%) with oral and dental POEs was therefore made up of patients with no history of dental interventions. It was assumed that these patients presented a deficient state of oral health in the form of dental, endodontal or periodontal infection (**Table 7**).

These results agree strongly with those of Lockhart et al. [11] who presented a comparative study on the presence of bacteraemia in patients undergoing tooth extractions and toothbrushing. They found that the risk of oral bacteraemia was significantly associated with poor oral hygiene during toothbrushing. However, they did not find any association in the extraction group, even when performed without antibiotic cover. This is consistent with statements that patients at risk of IE have greater exposure to the action of oral bacteria during activities of daily living, such as toothbrushing or chewing, particularly if the individual has poor oral hygiene.


**Table 7.** Infective endocarditis patients with identified oral and dental portals of entry (*n* = 68) [24].

These observations highlight the importance of maintaining oral hygiene in patients at highest risk of IE, and provide an important argument that dental care could have greater repercussions than antibiotic prophylaxis on the incidence of IE of oral origin.
