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Home All issues Volume 31 / No 3 (2025) J Oral Med Oral Surg, 31 3 (2025) 20 Full HTML
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J Oral Med Oral Surg
Volume 31, Number 3, 2025
Article Number 20
Number of page(s) 5
DOI https://doi.org/10.1051/mbcb/2025015
Published online 24 June 2025

© The authors, 2025

Licence Creative CommonsThis is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Introduction

Asthma is a respiratory disorder that affects more than 300 million individuals per year worldwide [1]. According to the World Health Organization, in 2019, asthma caused more than 450,000 deaths per year [2].

Asthma is among the most common respiratory diseases. It is caused by chronic inflammation of the airways, followed by respiratory tract hyperresponsiveness to various stimuli and narrowing of the airways [1,3]. Frequent symptoms include cough, wheezing, and dyspnoea [4,5].

While asthma can occur at a young age, it can also develop later in life and affects various age groups. The frequency of asthma-associated comorbidities increases with age. Older individuals present higher rates of morbidity and mortality as compared to younger patients [6]. These comorbidities can exacerbate respiratory symptoms, decrease quality of life, and worsen asthma control [7,8]. In Japan, approximately 90% of deaths due to asthma occur in adults aged 65 years or older [9].

Asthma and respiratory conditions were associated with certain oral diseases, mainly dental caries, dental erosion, periodontal diseases, and oral candidiasis [10–14]. In addition, certain oral diseases can affect the health of the respiratory system, which, in turn, can affect the oral microbiome [15].

The biological mechanisms underlying this association remain unclear, although a possible role for systemic inflammation and oxidative stress has been suggested [16]. It is plausible that chronic non-resolving inflammation and pro-inflammatory cytokines associated with asthma may disseminate via the vascular system, leading to elevated systemic inflammatory levels and contributing to the development and progression of oro-dental diseases.

Thus far, no studies have explored the possible association between asthma and acute periapical abscesses (PAs). Acute PAs present a severe health risk to patients and require expeditious and efficient treatment. More than 400,000 emergency patient visits in the United States were due to either pulpal or periapical diseases, resulting in medical charges totaling more than $160 million [17]. More than 60,000 hospitalizations were primarily attributed to periapical abscesses [18].

This cross-sectional study aimed to assess the prevalence of acute PAs in patients with asthma treated in a large medical facility in the United States.

Material and methods

Integrated data i2b2 of The University of Florida (UF), provided by the UF Health Office of the Chief Data Officer from October 2016 to May 2024, was used. The study complied with the UF IRB and Privacy rules for research on IRB-approved de-identified data sets. The UF Health Center Institutional Review Board (IRB) exempted the study as it did not include personal health information (PHI).

Data aggregated from 1,799,122 inpatients and outpatients visiting the UF Health Center were recorded using queries on the NIH and UF-supported platform i2b2. Diagnoses were coded using the international coding system ICD-10. The patient population analysed was mixed, presenting with different conditions, including acute PAs without sinuses and Asthma. Asthma was diagnosed based on medical history, physical examination obstruction during expiration, and lung functions (spirometry). Established patients were taking bronchodilators, steroids, or mast cell stabilisers.

Individual data was not analysed. However, all cases were diagnosed by calibrated, experienced oral healthcare professionals in a hospital setting for patients admitted to urgent care with symptoms of acute PAs. The calibrated dentists for ICD-10 codes followed the emergency clinic's strict diagnosis protocol.

Clinical examination and imaging data confirmed the diagnoses of acute PAs without sinus tract. Acute PA without a sinus is a dental infection where a collection of pus has formed at the periapical area of the root, resulting in pain and inflammatory reaction, but without a visible drainage to the outer surface. The aetiology is usually an infected pulp and the condition requires an emergency treatment. Acute PA in the affected patients was diagnosed by clinical and radiological examination combined with a thorough anamnesis from the patient.

Inclusion criteria encompassed all patients with the corresponding code for acute PAs without sinus (ICD-10: K04.7) and asthma (ICD-10: J45). There were no exclusion criteria since all codes were computerised, and specific diagnoses of acute PAs in the total hospital patient population were searched using the appropriate ICD-10 code. The history of PA and asthma was identified in the database by searching the appropriate query. Dental treatment included endodontic treatment and coronal restoration whenever the natural tooth was salvageable.

Patients with ICD-10 diagnosis codes of acute PAs were recorded, and the prevalence of acute PAs in patients with asthma was compared to the prevalence in the total hospital patient population.

The odds ratio (OR) of the prevalence of acute PAs and their association with the history of asthma were evaluated using a 95% confidence interval, and the statistical difference between the study groups was assessed using MEDCALC software. A standard normal deviation (z-value) was calculated as follows: ln(OR)/SE{ln(OR)}. The p-value was the normal distribution area outside ±z [19]. p-value < 0.05 was considered statistically significant.

Logistic regression was conducted for diabetes, smoking, and periodontal disease comorbidities using the aggregated counts as weight in the model, and adjustment for such comorbidities was made. SAS 9.4 PROC LOGISTIC procedure was used for the statistical evaluation.

The odds ratio (OR) of the prevalence of acute PAs and their association with asthma in the hospital patient population was calculated and analysed.

Results

Out of 1,799,122 patients analysed, 834,729 were males and 964,393 females (Tab. I). 2,237 patients presented with a history of both asthma and acute PAs (Tab. I). Patients with asthma showed significantly more PAs than patients without asthma (p < 0.0001) (Tab. II). Females were more affected than males at twice the rate; (Tab. I). There was no difference between whites and African Americans or between whites and African Americans combined with other ethnicities (Tab. I). Patients older than 18 were more affected than younger patients were nearly six times more likely (Tab. I).

The odds ratio (OR) for acute PAs in patients with asthma was 3.83, and the difference in prevalence as compared to the total hospital patient population was statistically significant (p <0.0001) (Tab. II). Following adjustment for diabetes mellitus comorbidity, the OR for acute PAs in patients with a history of asthma was 3.81, and the difference in prevalence as compared to the total hospital patient population was statistically significant (p <0.0001) (Tab. III). Following adjustment for smoking co-morbidity, the OR for acute PAs in patients with a history of asthma was 3.54, and the difference in prevalence as compared to the total hospital patient population was statistically significant (p <0.0001) (Tab IV). Following adjustment for periodontal disease co-morbidity of patients receiving urgent care treatment, the OR for acute PAs in patients with a history of asthma was 3.83, and the difference in prevalence compared with the total hospital patient population was statistically significant (p <0.0001) (Tab. V). There was no statistical difference between the OR for acute PAs in patients with asthma after adjustment for diabetes mellitus, smoking, and periodontal disease.

Table I

Demographic distribution of the hospital population studied (n=1,799,122). PAs=acute periapical abscesses.

Table II

Odds ratio (OR) for acute periapical abscesses (PAs) in hospital patients with asthma. CI=confidential interval.

Table III

Odds ratio (OR) for acute periapical abscesses (PAs) in hospital patients with asthma after adjustment for diabetes mellitus comorbidity. CI=confidential interval.

Table VI

Odds ratio (OR) for acute periapical abscesses (PAs) in patients with asthma after adjustment for smoking. CI=confidential interval.

Table V

Odds ratio (OR) for acute periapical abscesses (PAs) in patients with Asthma after adjustment for periodontal disease. CI=confidential interval.

Discussion

The results of this extensive cross-sectional study show that the prevalence of acute PAs in patients with asthma is higher than in those without this condition. This may offer new insight on the relationship between asthma and acute PAs.

Diabetes [20–21], smoking [22], and periodontal disease [23] were found to be significant comorbidities for acute PAs. Diabetes increases inflammation in the periodontal and periapical tissues, impairs new bone formation, and increases the expression of RANKL in response to microbial stimulation [20]. Cigarette smoking irritates the oral mucosa and changes microbial microbial flora and host resistance factors by reducing blood supply to the alveolar bone and potentially decreasing bone mineral density [24]. Periodontal pathogenic microorganisms or their toxic by-products invading the pulp can release inflammatory cytokines such as TNF-α, IL-1β, IL-6, and IL-10 that can detrimentally affect the pulp and periapical tissues [25]. This immune response includes factors that promote acute periapical abscesses (PAs) and apical bone resorption [26].

Even after adjusting for diabetes mellitus, smoking, and periodontal disease comorbidities, the odds ratios for acute PAs in patients with asthma remained high and statistically significant. This result suggests that the association between asthma and acute PAs may occur independently from these comorbid factors.

Oral microorganisms, including periodontal pathogens, have been identified as significant contributors to respiratory diseases. Good oral health is intimately related to good respiratory health; the reverse is also true. Various factors such as dietary habits, smoking, inadequate oral hygiene, certain diseases, and medications can induce dysbiosis in the oral microbiome. This disruption increases the presence of harmful and inflammatory microbes, which can penetrate the respiratory tract and lungs, leading to respiratory diseases such as influenza, asthma, COPD, and pneumonia [27]. Consequently, it severely impacts the quality of life of these patients [28]. This phenomenon was also observed in the association between periodontal disease and COVID-19 infection [29].

Etiologic factors of periapical infection share similarities with periodontal disease. Pathways for infection between the periodontium and the pulp can be dentinal tubules, lateral canals, and the apical foramen [30]. Periodontal disease and PAs reflect a host response to microbial invasion. Pathogenic microorganisms infecting the dental pulp release inflammatory cytokines such as TNF-α, IL-1β, IL-6, and IL-10, which affect the pulp and periapical tissues, promoting acute PAs and associated bone resorption [31,32].

Oral microbiome disruption can trigger both oral and respiratory diseases, further destabilising the balance of the oral microbiome. It creates a concerning cycle in which lung illnesses, oral disorders, and disruptions to the oral microbiota constantly exacerbate each other. Understanding and addressing this cyclical link is crucial for preventing lung and oral health deterioration.

The results of this cross-sectional study should be extrapolated with caution, and several limiting factors should be considered. This study was a cross-sectional study in one medical institution, and as such, it cannot establish a strict cause-and-effect relationship. In addition, the patient population examined may have had additional underlying systemic or dental conditions affecting the odds of acute PAs. Also, the quality of tooth restoration and endodontic treatment were not analysed. However, since diabetes, smoking, and periodontal disease are significant comorbidities that can affect the OR of PA development, adjusting for such comorbidities did not affect the OR significantly.

In addition, we did not adjust for the different classes of medications used to treat asthma. Asthma medication comprises bronchodilators, corticosteroids, and anticholinergic drugs. Most of these drugs are inhaled using various forms of inhalers. The effect of these drugs on oral health is the subject of debate. Patients taking asthma medication may be at risk of dental caries, dental erosion, periodontal diseases, and oral candidiasis, which may contribute to the development of PAs [33].

In conclusion, within the limitations, the odds of acute PAs are significantly higher in patients with asthma seeking treatment for pain due to acute PAs. Therefore, clinicians should be aware of the potential increased risk of acute PAs in such patients and mitigate it in asthma patients by providing rigorous dental and oral prevention measures.

Funding

This research did not receive any specific funding.

Conflicts of interest

The authors affirm that they have no financial affiliation (e.g., employment, direct payment, stock holdings, retainers, consultantships, patent licensing arrangements or honoraria), or involvement with any commercial organization with direct financial interest in the subject or materials discussed in the manuscript.

Data availability statement

The data that support the findings of this study will be available in the Integrated data i2b2 of the University of Florida at https://idr.ufhealth.org and the relevant dataset will be provided upon request.

Ethics approval

All procedures performed in this study complied with the ethical standards of the institutional research committee and Privacy rules for research on IRB approved de-identified data sets. Approval date: 6 April 2021.

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Cite this article as: Katz J, Rotstein I. 2025. Asthma and Acute Periapical Abscesses. J Oral Med Oral Surg. 31, 20. https://doi.org/10.1051/mbcb/2025015

All Tables

Table I

Demographic distribution of the hospital population studied (n=1,799,122). PAs=acute periapical abscesses.

In the text
Table II

Odds ratio (OR) for acute periapical abscesses (PAs) in hospital patients with asthma. CI=confidential interval.

In the text
Table III

Odds ratio (OR) for acute periapical abscesses (PAs) in hospital patients with asthma after adjustment for diabetes mellitus comorbidity. CI=confidential interval.

In the text
Table VI

Odds ratio (OR) for acute periapical abscesses (PAs) in patients with asthma after adjustment for smoking. CI=confidential interval.

In the text
Table V

Odds ratio (OR) for acute periapical abscesses (PAs) in patients with Asthma after adjustment for periodontal disease. CI=confidential interval.

In the text

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