year [Ref]

Study design



Bahekar, A.A., et al., 2007 [11]

Systematic review.

Literature revealed 5 prospective cohort studies, 5 case control studies, 5 cross-sectional studies. Individual studies were adjusted for confounding factors such as age, sex, diabetes mellitus, and smoking.

Prospective cohort studies indicated that individual with PD had a 1.14 times higher risk of developing CHD than controls. Case control studies showed great risk of developing CHD. Prevalence of CHD in cross-sectional studies significantly greater among individual with PD than in those without PD. Cohort studies showed 1.24 times increase risk of development of CHD in patients with <10 teeth.

Both the prevalence and incidence of CHD were significantly increased in PD. The PD must be a risk factor for CHD. Prospective studies required to prove the risk reduction with the treatment of PD.

Ioannidou, E., et al., 2006 [15]


English literature of periodontal treatment on CRP levels assessed, at least 2 months after periodontal treatment. The search conducted in MEDLINE between 1966 and July 2005 and Cochrane Central Register of Controlled Trials.

Literature yielded 814 citations of which 10 met the inclusion criteria. Meta-analysis of RCT included that the difference in serum CRP levels is not significantly different between the two arms. The single-cohort studies suggested that the difference on serum CRP levels was not significantly different before and after treatment.

Evidence indicated that systemic inflammation presented in patients with periodontal disease. RCT and single cohort studies do not support that periodontal treatment can reduce CRP levels.

Seymour, R.A., et al., 2003 [19]


The paper reviewed the effect of cardiovascular drugs on the periodontium and management of patients with periodontal diseases. The risk of infective endocarditis arising from periodontal procedures, and the inter-relationship between periodontal disease and CAD.

Stopping anticoagulant therapy prior to periodontal procedures is putting patients at a greater risk of thromboembolic disorders compared to the risk of prolonged bleeding. Spontaneous bacteraemia arising from a patient’s oral hygiene practices is more likely to be the cause of endocarditis than one-off periodontal procedures. The risk of death from penicillin appears to be greater than the risk of death arising from infective endocarditis.

CAD can interact with the periodontium. Further investigation must

Manage anticoagulant therapy and the risk from infective endocarditis.

Hokamura,K., et al., 2010 [56]


Clarify the involvement of Pg on the mechanisms of development of aortic intimal hyperplasia. Intravenous administration of Pg induced intimal hyperplasia in the mouse model with photochemical impairment of the femoral artery.

No changes identified in the mice without aortic impairment, even with Pg infection. S100A9 and the SMemb were significantly over expressed on surfaces of smooth muscle cells present in injured blood vessels. Increased expressions of S100A9 and SMemb proteins observed in aneurismal specimens obtained from Pg infected patients. Bacteremia induced by Pg leads to intimal hyperplasia associated with over expressions of S100A9 and SMemb.

Pg is a causative event in the development of aortic hyperplasia in periodontitis. Upregulation of the S100A9 by Pg is important event in development of intimal hyperplasia in aorta.

Hall, G., et al., 1993 [57]

Clinical study.

60 healthy patients randomized to receive placebo, penicillin-V (2 g), or amoxicillin 1 hour before dental extraction was performed. Blood samples for microbiological investigation collected before, during, and 10 minutes post surgery and processed by lysis filtration

The overall incidence of bacteremia after dental extraction was 95%, 90%, and 85%, respectively, for the 3 groups. For >90% of 126 strains of viridans streptococci tested, the MIC of penicillin-V and ampicillin were £0.125 mg/L

The protective effect of prophylactically administered penicillins must be due to interference with the steps in the development of endocarditis, other than the transient bacteremia that occurs initially.

Maharaj, B., et al., 2012 [59]

Clinical study.

160 patients for antimicrobial prophylaxis before dental extraction. Group A served as control, group B rinsed with chlorhexidene, group C took 3 g amoxicillin orally, group D took 600 mg clindamycin.

The proportion of patients who had post-extraction bacteraemia in groups A, B, C and D was 35%, 40%, 7.5% and 20%, respectively. The differences between the control and amoxicillin groups and between the chlorhexidine and amoxicillin groups were statistically significant.

None of the treatments prevented post-extraction bacteraemia and confirmed earlier reports that bacteraemia is not completely eliminated by antibiotics.