Abstract
Background
Periodontitis, a chronic inflammatory disease affecting the supporting structures of teeth, has been
associated with systemic diseases, including cardiovascular conditions. Periodontal medicine
emphasizes the role of periodontitis in systemic health through inflammatory mediators like C-
reactive protein (CRP) and fibrinogen. This study aims to evaluate the clinical and systemic effects of
phase I periodontal therapy in patients with chronic periodontitis compared to periodontally healthy
individuals.
Materials and Methods
This randomized controlled prospective cohort study included 60 systemically healthy participants
aged 30-60 years from Modern Dental College and Research Centre, Indore. The subjects were
divided equally into two groups: Group I: 30 periodontally healthy individuals with <20% bleeding on
probing (BOP). Group II: 30 chronic periodontitis patients with probing pocket depth (PPD) ≥4 mm in
≥30% of sites. Exclusion criteria included systemic illnesses, smoking, alcohol consumption, and BMI
≥ 25 kg/m². Clinical parameters measured were BOP, PPD, clinical attachment loss (CAL), and oral
hygiene index (OHI-S). Biochemical markers such as CRP and plasma fibrinogen were assessed pre-
and post-therapy. Group II received full-mouth scaling and root planing, with follow-up evaluations
after three weeks. Statistical analysis was performed using SPSS software, with a significance
threshold of p < 0.05.
Results
Bleeding on Probing (BOP): Group II had significantly higher BOP (1.00±0.00) than Group I
(0.22±0.03) (p = 0.00). BOP in Group II reduced to 0.31±0.35 after therapy (p = 0.00). Probing Pocket
Depth (PPD): Group II exhibited higher PPD (5.99±0.55 mm) compared to Group I (1.52±0.27 mm) (p
= 0.00). Post-treatment, PPD reduced to 3.54±1.48 mm (p = 0.00). Clinical Attachment Loss (CAL):
CAL in Group II was 6.15±0.51 mm, which significantly improved to 3.71±1.49 mm after therapy (p =
0.00). Serum CRP: CRP levels in Group II reduced from 1.99±1.05 mg/L to 1.71±0.62 mg/L after
therapy (p = 0.017). Plasma Fibrinogen: Group II exhibited higher fibrinogen levels (2.16±0.32 g/L)
than Group I (1.79±0.55 g/L) (p = 0.002). Post-treatment, fibrinogen levels decreased to 1.86±0.49
g/L (p = 0.003).
Conclusion
Phase I periodontal therapy significantly improved clinical periodontal parameters, including BOP,
PPD, and CAL, in patients with chronic periodontitis. The therapy also reduced systemic inflammatory
markers, including CRP and fibrinogen, highlighting the potential of periodontal treatment in
mitigating cardiovascular risks and systemic inflammation.
Keywords
Periodontitis, systemic inflammation, periodontal therapy, C-reactive protein, fibrinogen,
cardiovascular disease, chronic periodontitis, oral health.
Introduction
Willoughby Dayton Miller first coined the term "focus of infection" in 1891, followed by William
Hunter in 1900, who introduced the "focal infection theory." According to this theory, bacteria
present in the oral cavity not only affect teeth and periodontal tissues but also contribute to systemic
diseases such as arthritis, endocarditis, pneumonia, asthma, anemia, neuritis, brain abscess, and
kidney diseases (1). Despite initial acceptance, conflicting evidence led to the theory's rejection by
various authors (2). However, in 1996, Offenbacher introduced the term "Periodontal Medicine" at
the World Workshop, which focused on the connection between periodontal and systemic diseases
(3). Periodontal medicine emphasizes the evaluation of systemic pathologies and periodontitis in
both human and animal models. Research in the late 1980s highlighted a relationship between
periodontal disease and cardiovascular conditions, including myocardial infarction, coronary
atherosclerosis, and ischemic stroke [4,5].
Periodontitis, an inflammatory disease affecting the supporting structures of teeth, is caused by
specific microorganisms, leading to progressive destruction of the periodontal ligament and alveolar
bone (6). Severe periodontitis affects approximately 10-15% of adults aged 21-50 and about 30% of
those over 50 (7). The bacteria and inflammatory mediators produced in periodontitis can enter the
systemic circulation, potentially causing systemic tissue damage through metastatic injury (8). This
mechanism forms the basis for the association between periodontitis and systemic diseases. A
procoagulant state, marked by enhanced coagulation and thrombosis, plays a key role in vascular
disease by fostering atherogenesis, which is also influenced by infectious agents and pathogen
burden (9). Offenbacher et al. (1) suggested that both periodontitis and atherosclerosis share chronic
inflammatory processes, coining the term “periodontitis-atherosclerosis syndrome.”
Materials and Methods
This randomized controlled prospective cohort trial was conducted on 60 systemically healthy
subjects selected from patients visiting Modern Dental College and Research Centre, Indore. The
participants were divided equally into two groups: Group I included 30 periodontally healthy
individuals with less than 20% of sites showing bleeding on probing, while Group II consisted of 30
chronic periodontitis patients with probing pocket depth of 4 mm or more in at least 30% of sites.
The inclusion criteria involved systemically healthy individuals aged 30 to 60 years, with at least 20
teeth present and no history of periodontal treatment in the previous six months, willing to
participate in the study. Exclusion criteria included systemic illnesses such as diabetes or
cardiovascular disease, pregnant or lactating women, individuals with smoking, alcohol, or tobacco
habits, those undergoing pharmacological therapy, individuals with a family history of cardiac
disease, and those with a BMI ≥ 25 kg/m².
Clinical parameters assessed in the study included probing pocket depth (PPD), measured at four
sites per tooth (excluding third molars), and recession, measured from the gingival margin to the
cemento-enamel junction (CEJ). Clinical attachment loss (CAL) was calculated by summing recession
and PPD. Full-mouth bleeding scores (FMBS) were recorded to assess bleeding on probing (BOP), and
oral hygiene status was evaluated using Greene and Vermillion’s Simplified Oral Hygiene Index (OHI-
S). Biochemical markers were also analyzed, with 5 mL of blood collected from the median cubital
vein for hemogram, including hemoglobin levels, total and differential leukocyte counts, platelet
counts, and bleeding and clotting times. Serum C-reactive protein (CRP) was measured using a
turbidimetric method, and plasma fibrinogen was assessed using the Clauss method. Blood sugar
levels (random and fasting) were measured to rule out diabetes, and blood pressure (systolic and
diastolic) was recorded using a sphygmomanometer to exclude hypertension.
The treatment protocol involved no intervention for Group I, while Group II received full-mouth
scaling and root planing within 24 hours, followed by oral hygiene maintenance instructions. Clinical
and biochemical parameters were recorded at baseline for both groups and three weeks post-
treatment for Group II. All data were statistically analyzed using SPSS software. Inter-group and intra-
group comparisons of means were performed using the Student’s t-test, and categorical data were
analyzed with the chi-square test. Pearson’s correlation coefficient was used to determine the
association between variables, while multiple linear regression analysis evaluated the independent
impact of various factors. A p-value <0.05 was considered statistically significant.
Results
The study included 60 participants, with a mean age of 37.08±6.32 years, consisting of 39 males and
21 females. Participants were equally divided into two groups: periodontally healthy (Group I) and
chronic periodontitis patients (Group II). The mean age between the groups showed no significant
difference (p=0.952), and the sex distribution was also statistically non-significant (p=0.787).
Bleeding on Probing (BOP): The mean number of bleeding sites was significantly higher in Group II
(1.00±0.00) compared to Group I (0.22±0.03) (p=0.00). After periodontal therapy, BOP in Group II
significantly reduced from 1.00±0.00 to 0.31±0.35 (p=0.00).
Probing Pocket Depth (PPD): Mean PPD was significantly higher in Group II (5.99±0.55 mm)
compared to Group I (1.52±0.27 mm) (p=0.00). Post-therapy, PPD in Group II reduced significantly
from 5.98±0.54 mm to 3.54±1.48 mm (p=0.00).
Clinical Attachment Loss (CAL): Group II had significantly higher CAL (6.15±0.51 mm) compared to
Group I (0.00±0.00 mm) (p=0.00). After therapy, CAL in Group II decreased from 6.15±0.51 mm to
3.71±1.49 mm (p=0.00).
Oral Hygiene Index (OHI-S): Group II had a higher mean OHI-S score (3.12±0.46) compared to Group
I (0.91±0.18) (p=0.00). Post-therapy, Group II's OHI-S score decreased significantly from 1.46±0.46 to
0.86±0.21 (p=0.00).
Serum C-Reactive Protein (CRP) and Plasma Fibrinogen: CRP levels showed no significant difference
between the groups (p=0.428); however, a significant reduction was observed post-therapy in Group
II (p=0.017). Plasma fibrinogen was significantly higher in Group II (2.16±0.32 g/L) compared to
Group I (1.79±0.55 g/L) (p=0.002) and significantly decreased post-therapy (p=0.003).
Key Results in Tables
Parameter Group I (Healthy) Group II p-value
(Periodontitis)
Mean Age (years) 37.13±6.48 37.03±6.26 0.952
Mean BOP (sites) 0.22±0.03 1.00±0.00 0.00
Mean PPD (mm) 1.52±0.27 5.99±0.55 0.00
Mean CAL (mm) 0.00±0.00 6.15±0.51 0.00
Mean OHI-S 0.91±0.18 3.12±0.46 0.00
Mean Serum CRP (mg/L) 1.80±0.77 1.99±1.05 0.428
Mean Plasma Fibrinogen (g/L) 1.79±0.55 2.16±0.32 0.002
Parameter Baseline (Group II) 3 Weeks Post-Therapy (Group II) p-value
Mean BOP (sites) 1.00±0.00 0.31±0.35 0.00
Mean PPD (mm) 5.98±0.54 3.54±1.48 0.00
Mean CAL (mm) 6.15±0.51 3.71±1.49 0.00
Mean OHI-S 1.46±0.46 0.86±0.21 0.00
Mean Serum CRP (mg/L) 1.99±1.05 1.71±0.62 0.017
Mean Plasma Fibrinogen 2.16±0.32 1.86±0.49 0.003
(g/L)
Discussion
This study evaluated the clinical and biochemical effects of phase I periodontal therapy on patients
with chronic periodontitis, focusing on markers of pro-coagulant state and comparing them with
periodontally healthy individuals. The findings align with previous research, supporting the role of
periodontal disease as a systemic inflammatory burden and its potential association with
cardiovascular risks (1,2).
Periodontitis is characterized by chronic inflammation leading to periodontal tissue destruction,
which contributes to elevated levels of inflammatory markers like CRP and fibrinogen (3). In our
study, phase I periodontal therapy significantly reduced clinical parameters, including bleeding on
probing (BOP), probing pocket depth (PPD), and clinical attachment loss (CAL). The reduction in BOP
from 1.00±0.00 to 0.31±0.35 (p=0.00) and the decrease in PPD from 5.98±0.54 mm to 3.54±1.48 mm
(p=0.00) corroborate earlier studies showing the effectiveness of non-surgical periodontal treatment
in improving periodontal health (4). Additionally, the decline in CAL from 6.15±0.51 mm to 3.71±1.49
mm (p=0.00) further confirms the positive impact of scaling and root planing (5).
The relationship between periodontal disease and systemic inflammation is well-documented, with
CRP serving as a reliable marker for systemic inflammatory responses (6). Although the baseline CRP
levels between the two groups were not significantly different (p=0.428), a statistically significant
reduction was observed post-therapy in the chronic periodontitis group (from 1.99±1.05 mg/L to
1.71±0.62 mg/L, p=0.017). This decrease suggests that periodontal therapy can help reduce systemic
inflammation, consistent with other reports showing similar reductions in CRP after periodontal
treatment (7).
Fibrinogen, another key pro-coagulant marker, was significantly elevated in the periodontitis group
compared to healthy subjects (2.16±0.32 g/L vs. 1.79±0.55 g/L, p=0.002). Elevated fibrinogen levels
are associated with increased blood viscosity and thrombosis, contributing to cardiovascular disease
risk (8). The significant reduction in fibrinogen levels post-treatment (from 2.16±0.32 g/L to
1.86±0.49 g/L, p=0.003) aligns with previous studies, reinforcing the systemic benefits of periodontal
therapy in mitigating cardiovascular risks (9).
Although the platelet count and total leukocyte count did not differ significantly between the groups
at baseline, a reduction in leukocyte count was observed post-therapy (from 7251.83±1383.78 to
6961.90±1355.46, p=0.00). This finding is significant, as elevated leukocyte levels have been linked
with endothelial dysfunction and atherosclerosis (1). The observed reduction suggests that
periodontal therapy not only addresses local inflammation but also reduces systemic leukocyte
levels, which may help prevent vascular complications (2).
The study’s results further support the association between chronic periodontitis and systemic
conditions such as cardiovascular disease by highlighting the role of inflammatory and coagulation
markers. These findings align with the "periodontitis-atherosclerosis syndrome" concept proposed by
Offenbacher et al. (1), suggesting that periodontal and cardiovascular diseases share common
inflammatory pathways.
In conclusion, this study demonstrates that phase I periodontal therapy significantly improves both
clinical periodontal parameters and systemic markers of inflammation, including CRP and fibrinogen.
These results highlight the importance of periodontal care in promoting overall health and
potentially reducing cardiovascular risks. Further studies with larger sample sizes and long-term
follow-ups are recommended to confirm the sustained benefits of periodontal therapy on systemic
health.
References
1. Offenbacher S, Katz V, Fertik G, et al. Periodontal infection as a possible risk factor for
preterm low birth weight. J Periodontol. 1996;67(Suppl 10):1103-13.
2. Seymour GJ, Ford PJ, Cullinan MP, Leishman S, Yamazaki K. Relationship between periodontal
infections and systemic disease. Clin Microbiol Infect. 2007;13(Suppl 4):3-10.
3. Loos BG, van Dyke TE. The role of inflammation and genetics in periodontal disease.
Periodontol 2000. 2020;83(1):26-39.
4. Tonetti MS, Eickholz P, Loos BG, et al. Principles in prevention of periodontal diseases:
Consensus report of group 1 of the 11th European Workshop on Periodontology on effective
prevention of periodontal and peri-implant diseases. J Clin Periodontol. 2015;42(Suppl 16)
5. Kotsakis GA, Naughton D, Ortiz-Vigon A, et al. Effect of scaling and root planing on systemic
biomarkers: A meta-analysis of randomized controlled trials. J Clin Periodontol.
2015;42(9):799-812.
6. Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and
prevention. Circulation. 2003;107(3):363-9.
7. Teeuw WJ, Slot DE, Susanto H, et al. Treatment of periodontitis improves the atherosclerotic
profile: A systematic review and meta-analysis. J Clin Periodontol. 2014;41(1):70-9.
8. Fibrinogen Studies Collaboration. Plasma fibrinogen level and the risk of major
cardiovascular diseases and nonvascular mortality. JAMA. 2005;294(14):1799-809.
9. Paraskevas S, Huizinga JD, Loos BG. A systematic review and meta-analyses on C-reactive
protein in relation to periodontitis. J Clin Periodontol. 2008;35(4):277-90.
