The saliva functions as a multifaceted biofluid vital for conserving dental homeostasis. It provides lubrication, demonstrates antibacterial properties, accelerates remineralization processes, and buffers acids produced by microbial metabolism and nutritional depletion.1 Protective mechanisms depend on the pH of saliva as a whole and its buffering ability; adequate buffering reduces acidity after carbohydrate consumption, hence reducing the ecological niche for aciduric organisms and controlling demineralization and mucosal irritation.2 Conversely, the development of caries, mucosal disorders, and delayed wound healing in the oral cavity are linked to low salivary pH and condensed buffer capacity.1

Salivary parameters have been linked to dental caries and periodontal disease in a number of cross-sectional and case-control investigations. These studies have shown different but plausible associations between lower pH, poorer buffering capacity, and higher disease prevalence. Oral mucosal pathological lesions encompass a wide range of conditions, such as traumatic ulcers, opportunistic infections like candidiasis, premalignant lesions like leukoplakia, and inflammatory and ulcerative lesions like recurrent aphthous stomatitis (RAS) and oral lichen planus (OLP).3 There are many factors at play; the beginning, progression, or danger of recurrent infection of lesions may be influenced by the local biochemical environment, namely the pH and buffering capacity of saliva.4,5 There is a dearth of research on oral mucosal lesions, and the findings are inconsistent; some studies indicate that individuals with mucosal sickness have a lower mean salivary pH, while others show no discernible abnormalities. Changes in study demographics, lesion types, saliva collection techniques, and buffering capacity tests may be the cause of the inconsistent findings.6

Reliable measurement techniques are essential for comparing studies: resting (unstimulated) whole saliva collected in the morning after refraining from food/drink provides reproducible baseline measures; salivary pH is readily measured by calibrated digital pH meters; buffering capacity is commonly assessed with titration methods such as the Ericsson technique (addition of a fixed amount of dilute HCl and measurement after equilibration), or by commercial strip tests that categorize buffer capacity.7 Employing approaches that are both well-described and repeatable enables more meaningful comparisons to be made across groups and provides support for clinical translation.8

This cross-sectional study aims to clarify the correlation between resting salivary pH, buffering capacity (assessed by the Ericsson technique), and the occurrence and classification of oral pathological lesions in an adult clinical population. We posited that reduced salivary pH and impaired buffering capacity would correlate with increased likelihood of inflammatory or ulcerative lesions and opportunistic infections (e.g., candidiasis), even when accounting for smoking, systemic diseases, medication-induced xerostomia, and other confounding variablesd

This was cross-sectional observational research conducted at the Oral Medicine and Oral Maxillofacial Surgery department of the institution, after clearance from the institutional review board protocol # (1239/B-KMC dated 3rd Feb 2025). Individuals aged 18 to 70 who visited the clinic for any purpose throughout the recruiting period were solicited. Exclusion criteria: current antibiotic or antifungal treatment (within the last 2 weeks), active systemic infection, history of head and neck radiation, significant salivary gland surgery, or incapacity to grant informed permission. A convenience sample of 300 individuals was selected to provide sufficient subgroup sizes for prevalent lesion types and to identify modest effect sizes for mean pH/buffer capacity variations across groups (power estimates indicated >80% power to detect Cohen’s d = 0.4 at α = 0.05). Every participant was checked separately by two qualified dental surgeons. Cohen's kappa (κ = 0.82), which measures inter-examiner agreement for lesion detection, showed good reliability. When there was debate, a diagnosis was agreed upon. Lesions were grouped for analysis as: inflammatory/ulcerative (aphthous ulcers, erosive OLP), infectious (oral candidiasis), premalignant (leukoplakia, erythroplakia), traumatic ulcers, and others. For at least one hour and thirty minutes before to sample collection, participants did not eat, drink (apart from water), smoke, or do oral hygiene tasks. Between 9:00 and 11:30 AM, those who were seated and leaning forward had their whole unstimulated saliva collected. The saliva was subsequently allowed to collect in a sterile tube for a duration of 5 minutes. The pH of saliva was measured immediately using a calibrated digital pH meter, which has an accuracy of ±0.01 pH. The cushioning capability was assessed using the Ericsson titration technique. A capacity of 0.5 mL of saliva was admixed with 1.5 mL of 0.005 M HCl, vortexed, permitted to stand for 10 mins, and the final pH was restrained. Buffering aptitude was characterized into tertiles i.e. low, medium, high and allocated numerical scores in agreement with reputable protocols. This methodology follows reputable techniques. Continuous variables are expressed as mean ± standard deviation, while categorical variables are presented as counts and percentages. Group comparisons employed t-tests or ANOVA for continuous variables and chi-square tests for categorical variables. Logistic regression models estimated odds ratios (OR) for lesion presence based on pH (both continuous and dichotomized at the sample median) and buffer capacity (categorical), while controlling for age, sex, smoking, xerostomia, and systemic disease. Significance threshold is set at p < 0.05. Analyses conducted using SPSS version 28l

112 (37.3%) of participants had at least one mucosal lesion; the most common were ulcerative/inflammatory lesions. Mean salivary pH and buffer scores were significantly lower in participants with mucosal lesions vs no lesions (p < 0.001 for pH; p = 0.002 for buffer score) (Table 1) (Table 2).

Table 1. Baseline characteristics (n = 300)

Table 2. Salivary Parameters by lesion status

After adjustment, low buffering capacity and lower pH were independently associated with higher odds of ulcerative/inflammatory lesions. Smoking was not a significant predictor in adjusted models here. Leukoplakia and premalignant lesions did not show consistent associations with pH/buffering capacity in this sample (small numbers). Candidiasis was more common in the low buffering capacity tertile (proportion with candidiasis: low buffer 9%, medium 4%, high 1.5%; p = 0.01). (Table 3)

Table 3.

This cross-sectional analysis acknowledged an association amongst lower resting salivary pH and reduced buffering capacity with the existence of oral mucosal lesions, explicitly ulcerative/inflammatory lesions (aphthous ulcers, erosive OLP) and oral candidiasis. The outcomes backing the biological rationale that an acidic oral environment and compromised buffering may underwrite to mucosal irritation, hinder healing, endorse microbial dysbiosis, and assist opportunistic infections.

Salivary parameters and oral disease have been allied in various previous studies carried out. Although results differ by age and population, studies looking at caries and periodontal disease frequently show that increased caries experience is linked to lower salivary pH and buffer capacity. The data on oral mucosal illness is sparser and more inconsistent; some papers show that patients with mucosal lesions have lower salivary pH than controls, while others report nonsignificant changes. The results of this study are unswerving with prior research on salivary pH, buffering capacity, and their relationship with oral pathological conditions. The results of Can et al. (2025)9, who also observed lower pH values in individuals with oral inflammatory and pathological mucosal changes, are consistent with the discovery that adults with oral lesions showed considerably lower salivary pH. This propensity is also sustained by Kogawa's (2024)10 results, which show that people with oral mucosal illnesses, mainly oral lichen planus, have salivary profiles that are prominently more acidic than those of healthy people. The experimental decrease in buffering capability in our study aligns with the findings of Kogawa et al. (2024)11, which showed that patients experiencing xerostomia and connected oral lesions displayed a significantly condensed buffering capacity, thereby increasing their susceptibility to mucosal deterioration and epithelial irritation. Polyakova et al. (2024)12 further corroborated our findings, signifying that acidic saliva endorses the formation and determination of ulcerative lesions. Their research reputable a significant association between low salivary pH and moderated buffering capacity in relation to recurrent aphthous stomatitis. According to Mandinić et al. (2024)13, patients exhibiting leukoplakia and other precancerous lesions confirmed a reduction in pH and buffering capacity. Metabolic deviations in saliva may impact the pathogenesis of several soft-tissue diseases in the oral cavity. The outcomes gained align with previous studies carried out that acme the grave function of salivary pH and buffering apparatuses in continuing mucosal veracity and thwarting lesions.

The prime influence contributory to the incongruities perceived amongst studies is methodological heterogeneity. Dissimilarities exist in the assortment interval, discussed to as diurnal flux, as well as in pre-collection constrictions such as eating, smoking, and oral hygiene. Additionally, there are differences amongst stimulated and unstimulated saliva, along with variations in buffer assay approaches, which may include simple strip tests or quantitative titration procedures like the Ericsson approach.14 Strip tests provide practical results; however, they do not offer fine granularity. In contrast, quantitative titration typically results in greater accuracy for inter-study comparability.

Research employing standardized unstimulated collection and quantitative titration frequently identified subtle variations in buffering capacity, thereby endorsing the application of the Ericsson-style titration methodology.5

The observed effects are further influenced by variations in demographic characteristics, such as age distribution, systemic comorbidities, medication usage that affects salivary function, and the incidence of xerostomia.15 The relative disparities between the lesion and non-lesion groups may be lessened in cohorts that are enriched with older persons or those who have polypharmacy, since these groups may have lower mean buffer levels. Due to a lack of longitudinal research, it is difficult to determine if low pH/buffering is a sign of pre-existing mucosal illness and local inflammation or a cause of lesion formation. Larger trials with clinical outcomes, such lesion recurrence and healing duration, are required, however small prospective and interventional studies indicate that improving salivary buffering may reduce microbial load and maybe lessen symptom burden.16 Enzyme activity and the function of the epithelial barrier are directly impacted by decreased salivary pH. Additionally, decreased buffering ability results in extended tissue exposure to low pH values by impeding the neutralization of local acids generated by microbial metabolism and refluxed stomach contents. These conditions may result in delayed wound healing, secondary infections, such as Candida overgrowth, and epithelial breakdown. The discovered connection to candidiasis makes physiological sense. Acidic environments are ideal for the growth of Candida species, and symptomatic candidiasis often develops in cases of xerostomia, reduced salivary flow, or compromised buffering ability.17 Simple chairside assays of salivary pH and buffering capacity might be used as extra screening methods for individuals with recurring mucosal disease or unexplained oral lesions if they are validated prospectively. Patients with inadequate buffer capacity may benefit from targeted treatments, including topical buffering rinses, saliva-stimulating methods, xerostomia control, and enhanced infection surveillance.18,

Ulcerative oral lesions and candidiasis were more prevalent in those with lower resting salivary pH and buffering ability. Saliva testing may be a non-invasive method for diagnosing and treating reoccurring oral mucosal disorders; however, more longitudinal research is required to identify aetiology and therapeutic significance 

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