Review Article

Effects of Periodontal Therapy on Systemic Markers in Healthy Patients

Rachana Hegde*
Department of Periodontology, Roseman University of Health Sciences College of Dental Medicine, USA

*Corresponding author: Rachana Hegde, Department of Periodontology, Roseman University of Health Sciences College of Dental Medicine, USA

Published: 22 Jun, 2017
Cite this article as: Hegde R. Effects of Periodontal Therapy on Systemic Markers in Healthy Patients. J Dent Oral Biol. 2017; 2(8): 1055.


Objectives: Periodontitis is associated with increased in inflammatory markers, especially cytokines and these inflammatory markers in turn have been observed in individuals with various systemic diseases. Periodontal therapy has also been believed to induce bacteremia and is thought to be a risk factor for distant site infections such as infective endocarditis in susceptible individuals. There are also reports of deleterious effects of blood loss following a periodontal surgery. However, there is conflicting data that reflects lack of evidence suggesting strong causal association between periodontal therapy and its effects on inflammatory marker, bacteremia and blood loss. This literature review will assess systemic effects (cytokines, bacteremia and blood loss) of invasive periodontal therapy and dental implants in systemically healthy individuals.
Methods: A comprehensive MEDLINE/PubMed literature search was conducted in January 2012 on systemic effects of surgical periodontal therapy and dental implant therapy. Of the 227 articles identified from literature; 23 articles were identified as highly relevant for the purposes of this literature review and the findings of these selected articles are summarized based on the intervention received.
Results: Inflammatory markers, TNF-α, IL-6, CRP and fibrinogen, significantly increase up to 24 h. After periodontal therapy and reaches its baseline levels after 1 month. Circulating PMNs, erythrocytes and Hemoglobin decreases after therapy and returns to baseline levels at 7 days. Transient bacteremia in the range of 3.3% to 80.9% was found in patients undergoing periodontal therapy. This transient bacteremia was reported to increase significantly during the point of maximum trauma to the soft tissues. Despite individual variation of the extent, invasiveness and duration of periodontal surgery, blood loss after routine periodontal therapy remains below 500 ml.
Conclusion: This literature review identifies anecdotal reports on incidence of cardiovascular and other systemic events following periodontal treatment. It further concludes that the relationship between periodontal treatment, bacteremia and inflammatory markers is dynamic and not completely understood. Further research is required to understand the causative model of post periodontal therapy systemic events.


Chronic periodontitis is defined as an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment, and bone loss. It is characterized by pocket formation and/or gingival recession [1]. Although it is a disease that is initiated by bacteria and their components like lipopolysaccharide, host defense plays an important role in the pathogenesis and disease progression. Various pathogenic products stimulate a variety of host cells resulting in the expression of inflammatory cytokines. Subsequent cascade of events and alteration in host immune response leads to increased inflammatory cell recruitment and tissue destruction.
It is now known that people with periodontitis have increased systemic levels of acute phase proteins, plasma antibody levels, coagulation factor, total white blood cell count, neutrophils, C reactive protein (CRP), and cytokines such as INF-gamma (Interferon gamma), TNF-α (Tumor necrosis Factor-Alpha), IL (Interleukin)-1β, IL-2 and IL-6 [2-6]. Heightened inflammatory markers have been reported in patients with cardiovascular disease [7,8], adverse pregnancy outcomes [9], diabetes [10] and respiratory disease [11]. Periodontal disease has hence been epidemiologically associated with these adverse systemic outcomes.
Periodontal therapy has also been believed to induce bacteremia, which is considered a risk factor for distant site infections such as infective endocarditis in susceptible individuals. This led to the present American Heart Association recommendations of antibiotic prophylaxis before dental procedures [12]. These recommendations are based on data concerning surrogate measures of risk such as invasiveness of a dental procedure and degree of periodontal disease at surgical site. However, there is conflicting data that reflects lack of evidence suggesting strong causal association between dental procedure-induced bacteremia and infective endocarditis [13]. It is hypothesized that other factors such as host immune and inflammatory response may play a role in determining the systemic effects of invasive dental procedures [14].
The purpose of the present literature review is to assess the systemic effects of invasive periodontal therapy and dental implants in systemically healthy individuals.

Figure 1

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Figure 1
Changes in circulating levels of TNF-a, IL-6, CRP and Fibrinogen and leucocyte differential counts at 1, 7 and 30 days after periodontal therapy [3]. N=55 at each time point. Analysis performed by ANOVA for repeated measures. * P<0.01, * P<0.001.


To obtain information on systemic effects of surgical periodontal therapy and dental implant therapy, a comprehensive MEDLINE/ PubMed literature search was conducted in January 2017 using the phrases “Systemic effects of periodontal or implant surgery and inflammatory markers or cytokines or plasma proteins” and “Periodontal therapy and Bacteremia”. The literature searches yielded 327 articles published to date that were available in English; the author reviewed the abstracts from these 327 articles and selected a subset, attempting to meet the following criteria:
Study design
Randomized clinical trials or prospective studies.
Healthy adults with no known systemic complications. Studies that did not report the patients being systemically healthy were not included in this review.
Sample size
More than 10 patients. Articles reporting on single center experience; case reports were not included of the 327 articles identified from literature; there were few articles that were repeated in multiple searches and the actual number of unique articles is less than 327. Based on the above inclusion criteria, 33 articles were identified as highly relevant for the purposes of this literature review and Table 1 and 2 summarizes the findings of these selected articles literature.

Summary of Literature Review

D’Aiuto et al. [3] found that TNF-α, IL-6, CRP and fibrinogen significantly increases and reaches its peak 24 h (Day 1) after periodontal therapy, however it starts decreasing after 24 h and reaches its baseline levels only after 1 month. They also found that the PMNs decreased significantly 24 h after treatment and erythrocytes and hemoglobin level remained lower than normal levels even at day 7 after the treatment. The group later concluded that during the acute response to periodontal therapy, there was a broad concordance between markers of inflammation and endothelial function. Figure 1 summarizes the findings.
Similarly, Ide et al. [26] measured the inflammatory markers immediately after the treatment and found increased levels of both IL-6 and TNF-alpha within 60 min to 120 min post treatment, but no significant difference in the measured levels were noted by the same group at 6 weeks. Ushida et al. [31] found this effect to be greater in patients treated with full mouth debridement compared to quadrant wise mechanical debridement and hence recommended evaluating the risks and benefits of full mouth debridement in patients with higher circulating levels of these markers i.e., people at high risk for cardiovascular events. However, Bahrani et al. [14] found no significant differences in any of the cytokine levels between baseline and 1 h post extraction. But, they also reported that their subjects had high variability in baseline cytokine levels and their study lacked the power (n=41) to identify the existing differences in cytokine levels.

Table 1

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Table 1
Summary of effects on cytokines after periodontal therapy.

Table 2

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Table 2
Summary of bacteremia after periodontal and implant surgery.


Bacteremia occurs when bacteria enter the bloodstream transiently and can be detected by laboratory blood culture techniques. Numerous papers were found in literature citing the incidence of bacteremia after daily procedures including chewing and tooth brushing. However, very few papers were found emphasizing the association between bacteremia and periodontal surgery. Also, it was difficult to differentiate between the treatment groups “scaling and root planning” and “periodontal surgery”, since little information was available on the invasiveness of the “scaling and root planning” procedure. For the sake of completeness of this review, non-surgical periodontal procedure like full mouth scaling and root planning with sub gingival curettage are included in this review.
Bacteremia was found in patients undergoing periodontal therapy in the range of 3.3% to 80.9%. However, most studies concluded that this bacteremia is transient in nature and increases significantly during the point of maximum trauma to the soft tissues.


Following periodontal therapy, cascade of events occur that include bacteremia, increased circulating inflammatory markers and blood loss. It is empirical to understand the interaction between these factors to identify a new causal model of association between oral therapy and incidence of adverse systemic events like infective endocarditis.

Inflammatory Markers and Bacteremia

While bacteremia does occur as result of periodontal surgery, it is also evident that “everyday” procedures like chewing and tooth brushing also results in bacteremia [28]. Most of the literature available measures the percentage prevalence of bacteremia and not the intensity. The intensity of the inocula of disseminated bacteria found in humans is lower than the intensity of bacteremia that has been shown to be an important factor in the genesis of experimental animal endocarditis [38]. Hence, argument in the favor of periodontal manipulation being the cause of cardiovascular events still remains unproven.
It is also evident from the current review that there is a transient increase in the inflammatory markers especially IL-6, TNF-α and CRP after periodontal therapy. It is proposed that the mechanisms that lead to this increased systemic inflammatory burden in otherwise healthy individuals include: (a) the local, infection driven production of inflammatory mediators (IL-1, IL-6) “dumped” into systemic circulation [39,40]. (b) the ability of the periodontal pathogens and/ or their toxins to disseminate and thus induce a distant inflammatory response [41,42]. (c) a combination of the above.

Bacteremia and Blood Loss

A correlation was found between the duration of oral surgery, amount of blood loss and bacteremia. When the amount of blood loss was more than 50 ml and the duration of surgery exceeded 100 min, the incidence of bacteremia was higher [43]. There was a statistically significant difference in the incidence of blood cultures positive for organisms at both shorter (<3 min, P=0.04) and longer (>6 min, P=0.04) surgery times [44]. On the contrary, Takai et al. [45] found that there was no association between degree of surgical invasion and bacteremia. They concluded in their clinical trial of 237 patients that any transoral incision produces bacteremia, the risk increases if the site is infected.


The results from this literature review indicate that there are anecdotal reports on incidence of cardiovascular and other systemic events following periodontal treatment. The relationship between periodontal treatment, bacteremia and inflammatory markers is dynamic but not completely understood. Further research is required to understand this interplay and its effects on systemic health.


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