Oral health and subclinical vascular changes: a cross-sectional ultrasonographic study

Abstract

Background

Periodontitis and dental caries are prevalent oral diseases with potential systemic effects. Recent studies highlight a possible link between oral health and cardiovascular diseases via systemic inflammation and endothelial dysfunction. This study investigates the impact of periodontitis and dental caries on cardiovascular health by assessing their associations with carotid intima-media thickness (CIMT) and carotid arterial stiffness (CAS).

Methods

In this cross-sectional study, participants were classified to contrast two distinct oral inflammatory conditions: caries-free periodontitis and caries-affected periodontally healthy controls. Periodontal examinations and Decayed, Missing, and Filled Teeth (DMFT) scoring were performed. CIMT and CAS parameters, including distensibility coefficient (DC), compliance coefficient (CC), alpha stiffness index, beta stiffness index, and pulse wave velocity (PWV), were assessed using fully automated QIMT and QAS software based on high-resolution B-mode ultrasonography. Statistical analyses compared oral health parameters with cardiovascular markers.

Results

The periodontitis group exhibited significantly higher CIMT values, along with reduced DC and CC and increased β-stiffness index and PWV compared with periodontally healthy controls (p < 0.05). Periodontitis stage demonstrated significant correlations with CIMT and multiple arterial stiffness parameters, indicating a severity-dependent vascular effect. However, in age-adjusted linear regression models, periodontal group status was not independently associated with CIMT or carotid arterial stiffness parameters, whereas age remained a strong predictor across all vascular outcomes (all p < 0.001). Regarding dental caries, no significant associations were observed between total DMFT score and CIMT or arterial stiffness parameters. Although the missing teeth component showed a significant unadjusted correlation with CIMT, this association was no longer significant after adjustment for age and sex.

Conclusions

Although unadjusted analyses suggested worse CIMT and carotid stiffness profiles in periodontitis, age-adjusted models indicated that age was the dominant determinant of vascular parameters in this cohort. Dental caries showed no independent association with CIMT or carotid stiffness. The use of fully automated QIMT and QAS software enabled a comprehensive and operator-independent assessment of both structural and functional carotid properties, representing a key methodological contribution of this study.

Background

Periodontitis is a chronic multifactorial inflammatory disease caused by microorganisms and characterized by progressive destruction of the tooth supporting apparatus leading to tooth loss. Since 1989, numerous studies have suggested a potential link between periodontitis and systemic conditions such as cardiovascular and cerebrovascular diseases. The low-grade inflammation that is associated with periodontitis is hypothesised to contribute to atherosclerosis; however, the precise mechanisms underlying this relationship remain insufficiently elucidated [1].

Periodontitis is thought to affect vascular health through two primary mechanisms. The first is the direct pathway, in which bacteria and their endotoxins enter the bloodstream via inflamed periodontal tissues, triggering systemic immune responses that impair endothelial function and vascular integrity. The second mechanism is an indirect pathway, where periodontitis induces a systemic inflammatory response, leading to elevated levels of inflammatory mediators such as interleukin (IL)-8, IL-6, IL-1, and tumor necrosis factor (TNF)- α, all of which have been implicated in the pathogenesis of atherosclerosis [2].

Dental caries, another prevalent oral disease, is characterised by the demineralisation of tooth structures due to the production of acid by cariogenic bacteria within the oral biofilm. The primary bacterial species responsible for this process include Streptococcus mutans and Streptococcus sobrinus, which metabolise fermentable carbohydrates to produce lactic acid, leading to enamel and dentin demineralisation. Dental caries can increase systemic inflammatory burden, through the action of proinflammatory cytokines. Cytokines such as IL-1β and IL-6 are significantly overexpressed in pulp tissue exposed to carious dentin. Their elevated levels indicate an active immune response within the pulp, which can contribute to both local and systemic inflammation [3].

Elevated levels of TNF-α have been detected in the saliva of individuals with dental caries, particularly when combined with other systemic conditions such as obesity. This cytokine plays a crucial role in systemic inflammation and has been linked to various inflammatory diseases [4].

The Decayed, Missing, and Filled Teeth (DMFT) index is a widely utilised epidemiological tool for assessing dental caries status within populations. It provides a quantitative measure of caries prevalence and severity by recording the number of teeth that are decayed (D), missing due to caries (M), and filled (F).The DMFT index is of significant importance in public health and dental epidemiology, as it enables comparisons across different populations and facilitates the monitoring of oral health trends over time [5].

Cardiovascular health indicators such as carotid intima-media thickness (CIMT) and carotid arterial stiffness (CAS) have been the focus of considerable research in relation to systemic inflammation and chronic diseases. CIMT is a measure of the thickness of the intima and media layers of the arterial wall and serves as an early indicator of subclinical atherosclerosis. Increased CIMT has been shown to be associated with an elevated risk of cardiovascular events, and it is influenced by factors such as hypertension, ageing, dyslipidaemia, diabetes, smoking, obesity, and chronic inflammation [6]. The measurement of CIMT using B-mode ultrasound is a cost-effective and non-invasive method, and recent advancements in image processing techniques have enhanced its accuracy and efficiency. CAS, defined as the reduction in arterial elasticity leading to increased rigidity, is another important cardiovascular risk factor associated with conditions such as hypertension, stroke, and coronary artery disease. The stiffening of arteries is the result of a number of factors, including ageing, hypertension, atherosclerosis. All of these factors contribute to elevated blood pressure and an increased risk of cardiovascular morbidity [7]. A number of studies have identified chronic inflammation, dyslipidaemia, smoking, physical inactivity, diabetes, insulin resistance and chronic kidney disease as contributors to CAS [8]. Ultrasonography provides a reliable, non-invasive assessment of arterial stiffness by measuring both structural parameters and functional parameters. Several indices, including the Distensibility Coefficient (DC), Compliance Coefficient (CC), alpha index, beta index, and Pulse Wave Velocity (PWV), are commonly used to quantify arterial stiffness [9].

Although the association between periodontitis and subclinical atherosclerosis has been extensively studied using carotid intima–media thickness, the vascular implications of dental caries remain poorly understood, particularly with respect to arterial stiffness. Previous studies have largely relied on cumulative indices such as DMFT and CIMT, reporting inconsistent findings, and have not evaluated the relationships between individual DMFT components and CAS parameters. Moreover, ultrasonographic assessments in this field have predominantly employed manual or semi-automated techniques, which are susceptible to operator-dependent variability. To address these gaps, the present study employed fully automated ultrasound-based software to provide standardized assessment of both CIMT and CAS. By contrasting two distinct oral inflammatory profiles—caries-free individuals with periodontitis and caries-affected periodontally healthy controls—the study aimed to explore the potentially different vascular effects of periodontal and caries-related inflammatory burdens. Accordingly, the primary objective was to examine the associations between periodontitis severity and CIMT and CAS parameters, while secondarily evaluating the independent relationships between individual DMFT components and these vascular markers.

Methods

Study design and participants

This study was conducted on 71 individuals aged 18–63 years who attended a dentomaxillofacial radiology clinic. Participants were selected to enable an etiologic contrast between two prevalent oral inflammatory conditions with distinct biological characteristics. Accordingly, individuals were classified into two groups: (1) the periodontitis group (n = 39), consisting of patients with clinically diagnosed periodontitis without active dental caries (decayed teeth, D = 0), and (2) the control group (n = 32), consisting of periodontally healthy individuals with at least one active dental caries lesion (D ≥ 1). Periodontal health was defined by the absence of clinical attachment loss and the absence of radiographically detectable alveolar bone loss. This grouping strategy was adopted to minimize the overlap between periodontal and carious disease–related inflammatory burdens and to enable a clearer assessment of their potentially distinct associations with vascular parameters. Participants included in the study had a minimum of 10 permanent teeth. The remaining inclusion and exclusion criteria were applied uniformly to both groups.

Exclusion criteria included the presence of systemic diseases such as cardiovascular disease, cerebrovascular disease, diabetes mellitus, or dyslipidemia, the use of anti-inflammatory or antibiotic medications, history of non-surgical or surgical periodontal therapy in the preceding 6 months and a body mass index (BMI) greater than 35 kg/m². All participants provided written informed consent after receiving both verbal and written explanations of the study. All ultrasonographic and clinical examinations, including CIMT and CAS measurements, were performed by the author, a dentomaxillofacial radiology specialist with 9 years of experience. The study was conducted in accordance with the Declaration of Helsinki and received approval from the Clinical Research Ethics Committee (Decision No: 2024/16/17).

Anthropometric and clinical measurements

The participants’ height and weight were measured, and BMI (kg/m²) was calculated. Resting systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured using a calibrated aneroid sphygmomanometer (ERKA, Germany). Two consecutive measurements were taken, and the average value was used for analysis. Hypertension was defined as a patient-reported history of hypertension or use of antihypertensive medication, or an SBP of 140 mmHg or higher or a DBP of 90 mmHg or higher. Individuals with hypertension were excluded from the study. Dyslipidaemia was assessed based on lipid profile test results obtained within one month prior to the study. Dyslipidemia was defined as a total cholesterol level of 200 mg/dL or higher, Low-Density Lipoprotein (LDL) of 100 mg/dL or higher, triglycerides of 150 mg/dL or higher, or High-Density Lipoprotein (HDL) of 40 mg/dL or lower in males or 50 mg/dL or lower in females. Individuals with dyslipidemia were excluded from the study.

Periodontal examination and DMFT scoring

The periodontal evaluation was conducted in accordance with the 2017 Workshop of the American Academy of Periodontology criteria, with the staging of periodontitis being determined based on clinical attachment level (CAL), which was measured using a periodontal probe under an artificial light source, and radiographic bone loss, which was assessed on panoramic radiographs (Hyperion X5, MyRay, Italy). For group allocation, participants were classified according to the presence or absence of periodontitis. The staging of periodontitis ranged from Stage I (mild) to Stage IV (advanced) [10]. Periodontitis staging (Stage I–IV) was recorded to characterize disease severity and was subsequently used in correlation analyses with vascular parameters rather than as a primary grouping variable.

Dental caries status was assessed using the DMFT index in accordance with World Health Organization criteria. The DMFT score was calculated as the sum of decayed (D), missing (M), and filled (F) permanent teeth [11]. In the present study, DMFT scoring was used to characterize caries burden within the study population and to support control group definition, rather than as a primary grouping variable. This approach was chosen to distinguish between periodontal- and caries-related inflammatory profiles while avoiding overlap between the two conditions. In addition to the total DMFT score, the individual components (D, M, and F) were analyzed separately to explore their potential differential associations with vascular and stiffness-related parameters. For inclusion in the control group, the presence of at least one decayed tooth (D ≥ 1) was required.

CIMT measurement

CIMT was assessed using a high-resolution B-mode ultrasonography system (Esaote MyLabX7, Naples, ITALY) with an L4-15 linear probe. All measurements were performed using the device’s built-in fully automated CIMT measurement software Quality Intima–Media Thickness (QIMT) to ensure standardization and eliminate operator-dependent variability. Participants were requested to rest for a period of five minutes prior to measurement. Patients were placed in the supine position and the neck was turned at an angle of approximately 20° to the opposite side. The probe was placed perpendicular to the right common carotid artery (CCA) and a real-time image was obtained in the longitudinal plane. CIMT was measured along a 1 cm section proximal to the carotid bifurcation using the device’s automated CIMT measurement function. When the standard deviation of five consecutive measurements was 10 μm or less, the image was validated and saved to the PACS system (Fig. 1). No manual measurements were performed.

Fig. 1.

CIMT measurement performed using the device’s inbuilt automated software

CAS measurements

Carotid artery stiffness parameters were obtained using the fully automated QAS (Quality Arterial Stiffness) geometric analysis software integrated into the Esaote MyLabX7 ultrasound system. The automated software analyzed arterial wall motion during systole and diastole to calculate stiffness indices, eliminating potential human error associated with manual measurements (Fig. 2). Standard deviation thresholds of ≤ 10 μm were applied to ensure accuracy. The following formulae were used for these measurements:

Fig. 2.

CAS measurements performed using the device’s inbuilt automated software

Compliance Coefficient (CC): CC quantifies the absolute change in arterial volume or cross-sectional area per unit change in pressure. It indicates the ability of an artery to expand with increasing pressure; higher compliance suggests more elastic arteries.

Distensibility Coefficient (DC): DC measures the relative change in arterial volume or cross-sectional area in response to pressure changes, reflecting the elasticity of the arterial wall. A higher DC indicates more elastic (less stiff) arteries.

Alpha Stiffness Index (α): ​The alpha index is a parameter used to assess arterial stiffness, particularly focusing on the relationship between arterial pressure and volume changes.

Beta Stiffness Index (β): The beta-stiffness index is a dimensionless parameter that evaluates arterial stiffness independent of blood pressure. It is calculated using the natural logarithm of systolic-to-diastolic pressure ratio divided by the relative change in arterial diameter. A higher beta index indicates increased arterial stiffness.

Pulse Wave Velocity (PWV): PWV measures the speed at which pressure waves move through the arterial tree. PWV is widely accepted as a key indicator of arterial stiffness, with higher PWV values corresponding to increased arterial rigidity.

Statistical analysis

The data were analysed using IBM SPSS 26.0 (Statistical Package for the Social Sciences). In the statistical analysis phase, firstly, descriptive statistics related to the demographic characteristics of the patients were given. Subsequently, the Shapiro-Wilk and Kolmogorov-Smirnov normality tests were applied in order to determine the test statistics to be used. The independent sample t-test was employed for two independent groups exhibiting normal distribution, while the Mann-Whitney U test was utilised for the purpose of comparison between two independent groups lacking normal distribution. Categorical variables were compared using the chi-square test. Associations between quantitative variables that did not show normal distribution were assessed using Spearman’s rank correlation coefficient. To account for potential confounding effects, multivariable linear regression analyses were performed for variables showing significant unadjusted associations, with age and sex included as covariates. A power analysis was conducted using G*Power version 3.1, with an alpha level of 0.05 and a power of 0.80, to justify the sample size. A p-value < 0.05 was considered statistically significant for all analyses.

Results

A total of 71 individuals were included in the study, of whom 42.3% were male and 57.7% were female. The overall mean age of the study population was 35.77 ± 11.16 years. The mean age was higher in the periodontitis group (39.85 ± 10.60 years) compared with the control group (30.81 ± 9.86 years). Mean BMI was 26.98 kg/m² in the periodontitis group and 25.40 kg/m² in the control group, with no statistically significant difference between groups (p = 0.184).

Comparisons of CIMT and CAS parameters between the periodontitis and control groups are presented in Table 1. The periodontitis group exhibited significantly higher CIMT values compared with the control group (638.97 ± 125.27 μm vs. 592.45 ± 103.84 μm, p = 0.019).

Table 1.

Comparison of CIMT and CAS Measures Between Groups

		Mean	SD	Median	Min	Max	P-value
CIMT(μm)
	Periodontitis	638.97	125.27	630.00	314.00	1104.00	0.019*
	Control	592.45	103.84	575.00	368.00	969.00
CAS
	DC
	Periodontitis	0.02	0.01	0.03	0.01	0.05	0.004*
	Control	0.03	0.01	0.03	0.01	0.09
	CC
	Periodontitis	1.00	0.46	0.95	0.13	2.62	0.002*
	Control	1.28	0.59	1.25	0.16	3.29
	α
	Periodontitis	4.79	4.52	3.98	1.70	34.67	0.075
	Control	3.42	1.76	2.97	0.07	11.05
	β
	Periodontitis	11.10	12.04	8.21	1.78	73.58	0.003*
	Control	6.72	3.54	5.88	0.22	22.31
	PWV(m/s)
	Periodontitis	6.82	2.65	6.19	4.16	21.34	0.006*
	Control	5.78	1.58	5.51	3.28	11.82

CIMT carotid intima-media thickness

CAS carotid arterial stiffness

DC Distensibility Coefficient

CC Compliance Coefficient

α Alpha Stiffness Index

β Beta Stiffness Index

PWV Pulse Wave Velocity

SD standard deviation

Min minimum

Max maximum

*Statistically significant (p < 0.05)

In terms of arterial stiffness, DC and CC values were significantly lower in the periodontitis group (p = 0.004 and p = 0.002, respectively). Conversely, β and PWV values were significantly higher in individuals with periodontitis compared with periodontally healthy controls (p = 0.003 and p = 0.006, respectively). No statistically significant difference was observed between groups for the alpha stiffness index (α) (p = 0.075).

Given the significant age difference between the periodontitis and control groups, age-adjusted linear regression analyses were performed to evaluate whether group-related differences in vascular parameters were independent of age (Table 2). In these models, age emerged as a strong and consistent predictor of CIMT and all carotid arterial stiffness parameters (all p < 0.001). After adjustment for age, periodontal group status was no longer independently associated with CIMT, DC, CC, α-stiffness index, β-stiffness index, or PWV.

Table 2.

Age-adjusted linear regression results for vascular parameters

Outcome	Group β	Group p	Age β	Age p	Adj. R²
CIMT	−0.099	0.922	0.512	< 0.001*	0.241
DC	−0.339	0.735	−0.678	< 0.001*	0.352
CC	−0.544	0.588	−0.602	< 0.001*	0.292
α	0.168	0.867	0.489	< 0.001*	0.183
β	0.255	0.212	0.371	< 0.001*	0.116
PWV	0.307	0.759	0.503	< 0.001*	0.244

β standardized regression coefficient

Adj. R² adjusted coefficient of determination

CIMT carotid intima–media thickness

DC distensibility coefficient

CC compliance coefficient

α alpha stiffness index

β beta stiffness index

PWV pulse wave velocity

The relationship between periodontitis stage and vascular parameters is summarized in Table 3. Periodontitis stage demonstrated a significant positive correlation with CIMT (r = 0.400, p = 0.012), alpha stiffness index (r = 0.384, p = 0.016), beta stiffness index (r = 0.377, p = 0.018), and PWV (r = 0.421, p = 0.008). In contrast, a significant negative correlation was observed between periodontitis stage and CC (r = − 0.324, p = 0.044). No significant association was detected between periodontitis stage and DC (p = 0.081).

Table 3.

Correlation Between Periodontitis Stage and CIMT, CAS

Variable	Correlation Coefficient (r)	P-value
CIMT	0.400	0.012*
DC	-0.283	0.081
CC	-0.324	0.044*
α	0.384	0.016*
β	0.377	0.018*
PWV	0.421	0.008*

CIMT carotid intima-media thickness

CAS carotid arterial stiffness

DC Distensibility Coefficient

CC Compliance Coefficient

α Alpha Stiffness Index

β Beta Stiffness Index

PWV Pulse Wave Velocity

*Statistically significant (p < 0.05)

The correlations between DMFT components and CIMT and arterial stiffness parameters are presented in Table 4. Among the DMFT components, only the missing teeth component (M) showed a significant positive correlation with CIMT in the unadjusted analysis (r = 0.602, p < 0.001). No other significant correlations were identified between DMFT components or total DMFT score and CIMT or arterial stiffness parameters.

Table 4.

Spearman Correlation Between DMFT Components and CIMT and CAS Parameters

Variable	CIMT r P- value	DC r P- value	CC r P- value	α r P- value	β r P- value	PWV r P- value
D (decay)	-0.264 p = 0.145	+ 0.212 p = 0.298	+ 0.224 p = 0.271	-0.207 p = 0.311	-0.196 p = 0.337	-0.163 p = 0.427
M (missing)	+ 0.602 p = 0.00027*	-0.129 p = 0.531	-0.086 p = 0.677	-0.028 p = 0.890	-0.041 p = 0.844	+ 0.188 p = 0.357
F (filling)	+ 0.167 p = 0.361	-0.105 p = 0.609	-0.099 p = 0.630	+ 0.036 p = 0.862	+ 0.024 p = 0.907	+ 0.113 p = 0.582
DMFT (D + M+F)	+ 0.071 p = 0.698	-0.037 p = 0.842	+ 0.016 p = 0.939	-0.214 p = 0.240	-0.025 p = 0.893	+ 0.214 p = 0.498

CIMT carotid intima-media thickness, DC Distensibility Coefficient, CC Compliance Coefficient, α Alpha Stiffness Index, β Beta Stiffness Index, PWV Pulse Wave Velocity

*Statistically significant (p < 0.05)

To evaluate whether the observed associations were independent of age and sex, multivariable regression analyses adjusted for age and sex were performed (Table 5). After adjustment, the previously observed association between missing teeth (M) and CIMT was no longer statistically significant (p = 0.279). No consistent independent associations were identified between DMFT or its components and CIMT or carotid arterial stiffness parameters. Borderline statistical significance was observed for the associations between total DMFT score and α and β stiffness indices; however, these findings were not consistent across other stiffness parameters.

Table 5.

Age- and Sex-Adjusted Regression Analysis of DMFT Components and Vascular Parameters

Variable	CIMT	DC	CC	α	β	PWV
D (Decay)	-9.533 (6.513), β=-0.278, p = 0.143	+ 0.000 (0.001), β=+0.003, p = 0.988	-0.005 (0.048), β=-0.022, p = 0.913	-0.003 (0.163), β=-0.004, p = 0.987	+ 0.002 (0.327), β=+0.001, p = 0.996	-0.016 (0.132), β=-0.027, p = 0.906
M (Missing)	+ 22.897 (21.157), β=+0.479, p = 0.279	+ 0.002 (0.004), β=+0.276, p = 0.672	+ 0.080 (0.161), β=+0.281, p = 0.620	-0.246 (0.500), β=-0.295, p = 0.623	-0.501 (1.009), β=-0.299, p = 0.619	-0.118 (0.440), β=-0.169, p = 0.789
F (Filling)	+ 2.858 (4.661), β=+0.103, p = 0.540	+ 0.000 (0.001), β=+0.090, p = 0.590	+ 0.020 (0.033), β=+0.114, p = 0.551	-0.059 (0.084), β=-0.116, p = 0.486	-0.124 (0.171), β=-0.122, p = 0.469	-0.035 (0.067), β=-0.083, p = 0.600
DMFT (D + M+F)	+ 1.783 (2.986), β=+0.094, p = 0.551	+ 0.000 (0.000), β=+0.175, p = 0.238	+ 0.024 (0.017), β=+0.203, p = 0.148	-0.078 (0.039), β=-0.223, p = 0.047*	-0.159 (0.081), β=-0.226, p = 0.050	-0.045 (0.035), β=-0.155, p = 0.198

CIMT carotid intima-media thickness, DC Distensibility Coefficient, CC Compliance Coefficient, α Alpha Stiffness Index, β Beta Stiffness Index, PWV Pulse Wave Velocity

*Statistically significant (p < 0.05)

Discussion

The relationship between periodontal diseases and subclinical atherosclerosis has been the subject of extensive research, with CIMT serving as a crucial indicator in these studies. CIMT has been shown to be a valid marker for the detection of early atherosclerosis and cardiovascular disease in the absence of clinical symptoms [12]. Periodontitis, characterised by chronic inflammation and bacterial infection, has systemic effects beyond the oral cavity, influencing vascular health and potentially contributing to atherosclerosis development [1].

One of the primary mechanisms linking periodontitis to cardiovascular health is chronic inflammation. Pathogenic bacteria such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans can trigger a systemic inflammatory response. This response is mediated by pro-inflammatory cytokines, including IL-1, IL-6, TNF-α, which are elevated in individuals with periodontitis [13]. These cytokines contribute to endothelial dysfunction, a precursor to atherosclerosis, thereby increasing the risk of coronary heart disease. Additionally, periodontal inflammation can elevate C-reactive protein (CRP) and fibrinogen levels, both of which are systemic inflammatory markers associated with cardiovascular events [14]. Another potential mechanism is transient bacteremia, where periodontal pathogens enter the bloodstream during routine activities such as chewing or brushing teeth [15]. Oral bacteria have been detected in cardiovascular tissues, suggesting a direct link between periodontal pathogens and cardiovascular disease [16]. Typically, CIMT ranges from approximately 0.4–0.5 mm in childhood, progressively increasing with age. Values exceeding 1.0 mm are considered abnormal, indicating elevated cardiovascular risk [17]. Previous studies have demonstrated a correlation between increased periodontitis severity and elevated CIMT. Beck et al. reported that severe periodontitis increased the probability of a CIMT greater than 1 mm by approximately 30% [18]. Similarly, Tsai et al. observed higher CIMT values corresponding with increased periodontal disease severity, supporting the hypothesis that systemic inflammation from periodontal disease contributes to carotid atherosclerosis [19]. Consistent with previous reports, our unadjusted analyses demonstrated higher CIMT values in the periodontitis group compared with controls. In addition, periodontitis severity showed a positive association with CIMT in correlation analyses. However, these findings should be interpreted with caution, as age-adjusted models indicated that age was the primary determinant of CIMT, suggesting that the observed associations largely reflect age-related vascular remodeling rather than an independent effect of periodontitis.

However, some studies report conflicting results. For instance, Lopez-Jornet et al. noted paradoxically lower CIMT in periodontitis patients compared to controls, a discrepancy potentially attributable to methodological differences, study population characteristics, or sample sizes [20]. Furthermore, Kida et al. emphasized that hypertension strengthens the association between periodontitis and increased CIMT, highlighting the need to consider systemic health factors when examining these relationships [21].

Periodontal inflammation may also directly contribute to arterial stiffness, a key indicator of cardiovascular health. Prior studies, including those by Iwasaki et al. and Jockel-Schneider et al., found that measures of arterial stiffness, PWV, were elevated in periodontitis patients [22, 23]. Similarly, systematic reviews and studies by Schmitt et al., Sanz-Miralles et al., and Ollikainen et al. consistently support a positive correlation between periodontitis severity and arterial stiffness [24, 25, 26]. Torumtay Cin’s research further emphasizes the impact of comorbidities, such as diabetes, amplifying the cardiovascular consequences of periodontitis [27]. The findings of this study are in alignment with the aforementioned reports, which demonstrate that arterial flexibility, as measured by the DC and CC, was reduced in patients suffering from periodontitis. This finding is indicative of increased arterial stiffness. Elevated PWV and β values, together with stage-dependent increases in α-stiffness, further confirmed increased arterial rigidity associated with advanced periodontitis stages. However, it should be noted that these observations were derived from unadjusted analyses. Given the strong influence of age on arterial stiffness, subsequent age-adjusted models indicated that age was the primary determinant of stiffness parameters, suggesting that the observed associations largely reflect age-related vascular changes rather than an independent effect of periodontitis.

An important methodological strength of the present study is the use of fully automated ultrasound-based analysis for both CIMT and carotid arterial stiffness measurements. Unlike earlier studies that predominantly employed manual techniques, the QIMT and QAS software packages provide automated wall detection, tracking, and parameter computation, thereby minimizing operator-related variability and enhancing reproducibility. This standardized approach may partially explain discrepancies between previous reports and the present findings, particularly with respect to subtle associations involving dental caries.

DMFT index is a widely used measure of dental health [28]. Several studies have explored the association between DMFT and CIMT, suggesting a potential link between poor oral health and cardiovascular risk. Uyar et al. expanded on these findings by evaluating 550 patients and assessing both carotid and popliteal artery intima-media thickness. They found that higher DMFT scores and Silness-Loe plaque index (SLI) scores correlated with increased intima-media thickness in both arteries [29]. Schillinger et al. also identified a significant relationship between high DMFT scores and carotid stenosis progression, indicating that poor dental health could contribute to subclinical atherosclerosis and even mortality risk in asymptomatic patients with carotid atherosclerosis [30].

However, conflicting evidence exists in the literature. Malvicini et al. conducted a case-control study that revealed no significant association between the DMFT index and cardiovascular variables [31]. Consistent with these latter findings, the present study did not detect any statistically significant relationship between DMFT scores and either CIMT or arterial stiffness parameters. Moreover, to the best of our knowledge, there has been no prior research explicitly evaluating the relationship between dental caries and arterial stiffness. Although inverse associations were observed between total DMFT score and α and β stiffness indices, these findings were borderline in magnitude, not consistent across other arterial stiffness parameters, and attenuated after adjustment for age and sex, suggesting a lack of clinically meaningful vascular effect of dental caries burden as assessed by DMFT.

Conclusion

In this cross-sectional ultrasonographic study, unadjusted analyses demonstrated less favorable carotid intima–media thickness and arterial stiffness profiles in individuals with periodontitis compared with periodontally healthy controls. However, age-adjusted regression analyses revealed that age was the dominant determinant of both CIMT and CAS parameters, and periodontal group status was not independently associated with vascular outcomes after adjustment. These findings indicate that the observed group differences are largely attributable to age-related vascular remodeling rather than an independent effect of periodontitis.

With respect to dental caries, neither total DMFT score nor its individual components showed an independent association with CIMT or carotid arterial stiffness after adjustment for age and sex. Although an unadjusted correlation between missing teeth and CIMT was observed, this association was attenuated after age adjustment, underscoring the confounding influence of age. These results suggest that cumulative caries indices may be insufficient to capture biologically active inflammatory phenotypes relevant to vascular changes.

Importantly, the use of fully automated QIMT and QAS software enabled standardized, operator-independent assessment of both structural and functional carotid parameters, representing a key methodological strength of this study. This automated approach enhances measurement reproducibility and provides a robust framework for future research.

Overall, the findings highlight the critical importance of accounting for age when evaluating oral–vascular associations and underscore the need for longitudinal, age-balanced studies incorporating refined oral disease phenotyping to clarify whether specific inflammatory profiles contribute independently to vascular remodeling and long-term cardiovascular risk. The cross-sectional design of the study and the relatively small sample size represent important limitations, as they preclude causal inference and may limit the generalizability of the findings.

Abbreviations

CIMT

Carotid Intima-Media Thickness

CAS

Carotid Arterial Stiffness

DMFT

Decayed, Missing, Filled Teeth

DC

Distensibility Coefficient

CC

Compliance Coefficient

PWV

Pulse Wave Velocity

IL

Interleukin

TNF

Tumor Necrosis Factor

BMI

Body Mass Index

CCA

Common Carotid Artery

CRP

C-Reactive Protein

SLI

Silness-Löe Index

Author’s contributions

E.S. conceptualized and designed the study, performed all ultrasonographic examinations (carotid intima-media thickness and carotid arterial stiffness measurements) as a dentomaxillofacial radiology specialist, conducted data analysis, interpreted the results, and wrote the manuscript.

Funding

This research received no external funding.

Data availability

The datasets used in the current study are available from the corresponding author upon request.

Declarations

Ethics declaration

The Clinical Research Ethics Committee (Decision No: 2024/16/17) approved the study. All procedures performed for the study were conducted in accordance with the tenets of the Declaration of Helsinki. Prior to the acquisition of radiological images, written informed consent was obtained from patients, who stated that the images may be used for scientific research. Consent forms are stored in the departmental archive.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.