Skip Navigation
Skip to contents

Restor Dent Endod : Restorative Dentistry & Endodontics

OPEN ACCESS

Articles

Page Path
HOME > Restor Dent Endod > Ahead-of print articles > Article
Research Article Prevalence of periapical abscesses in psoriasis patients: a retrospective cross-sectional study
Ilan Rotstein1,*orcid, Joseph Katz2orcid, Simone Grandini3orcid, Giulia Malvicini3orcid, Franklin Garcia-Godoy4orcid
Restor Dent Endod [Epub ahead of print]
DOI: https://doi.org/10.5395/rde.2026.51.e39
Published online: August 10, 2026

1Department of Endodontics and Periodontics, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA

2Department of Oral Medicine, Oral Diagnostic Sciences, University of Florida College of Dentistry, Gainesville, FL, USA

3Unit of Endodontics and Restorative Dentistry, Department of Medical Biotechnologies, University of Siena, Siena, Italy

4Department of Bioscience Research, University of Tennessee Health Science Center, College of Dentistry, Memphis, TN, USA

*Correspondence to Ilan Rotstein, DDS Department of Endodontics, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA 90007, USA Email: ilan@usc.edu

Citation: Rotstein I, Katz J, Grandini S, Malvicini G, Garcia-Godoy F. Prevalence of periapical abscesses in psoriasis patients: a retrospective cross-sectional study. Restor Dent Endod 2026;51(3):e39.

• Received: December 21, 2025   • Revised: February 8, 2026   • Accepted: March 29, 2026

© 2026 The Korean Academy of Conservative Dentistry

This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

  • 14 Views
  • 3 Download
  • Objective
    This study was performed to assess the prevalence of acute periapical abscesses (PAs) in patients with psoriasis and to determine whether this relationship remains after adjusting for related systemic, behavioral, and treatment-related confounders.
  • Methods
    A retrospective hospital-based analysis of 2,108,676 patients was conducted using de-identified clinical data. Diagnoses of psoriasis and acute PA without sinus involvement were identified using standardized coding. The association between psoriasis and acute PAs was assessed using odds ratios (ORs) with 95% confidence intervals (CIs). Multivariable logistic regression analyses were performed to adjust for diabetes, nicotine dependence, alcohol-related disorders, and biologic therapy use.
  • Results
    Among 16,084 patients with psoriasis, 224 were diagnosed with acute PAs. Psoriasis was associated with a significantly higher prevalence of acute PAs than in the overall hospital population (OR, 2.21; 95% CI, 1.94–2.53; p < 0.0001). This association remained statistically significant after adjustment for diabetes (OR, 1.40), nicotine dependence (OR, 1.31), alcohol related disorders (OR, 1.89), and biologic therapy use (OR, 1.77). Female patients and white patients with psoriasis exhibited a higher prevalence of acute PAs compared with other demographic groups.
  • Conclusions
    Psoriasis is independently associated with an increased risk of acute PAs, even after accounting for common medical and behavioral risk factors. Greater awareness among clinicians and closer collaboration between dermatology and oral healthcare providers can facilitate earlier diagnosis and preventive treatment.
Psoriasis is a chronic inflammatory skin disease. It presents a global health concern affecting more than 60 million individuals worldwide [1,2]. It impacts both men and women equally and can manifest at any age. The cost of psoriasis care in the United States exceeds $100 billion per annum [3].
Psoriasis is characterized by rash, itchy, and scaly patches most commonly found on the scalp, elbows, knees, and trunk. The condition is cyclic, alternating between flare-ups and remission, which often causes discomfort [1]. Cycle lengths vary by person and are not always predictable.
The etiology of psoriasis is genetic [1]. Psoriasis can be associated with multiple factors such as infections, stress, depression, trauma, smoking, obesity, excessive alcohol consumption, certain systemic diseases, and medications [112]. Psoriasis has no cure [1]. Treatment focuses on symptom management, flare reduction, and lifestyle modifications [1].
Psoriasis can be divided into the following groups [13,14]: (1) psoriasis vulgaris, also known as plaque psoriasis, is the most common type; (2) guttate psoriasis; (3) inverse psoriasis; (4) pustular psoriasis; and (5) erythrodermic psoriasis. Different pathological mechanisms were associated with each psoriasis type [13,1517].
An acute periapical abscess (PA) poses a health risk to patients and requires emergency treatment. In the United States, over 400,000 emergency room visits, resulting in more than $160 million in charges, were attributed to pulpal or periapical dental infections [18]. In addition, more than 60,000 hospitalizations were recorded [19].
An association between psoriasis and dento-oral diseases has been suggested [20,21]. Periodontal disease was commonly associated with psoriasis [2226]. However, additional information is needed regarding a potential association between psoriasis and periapical disease, mainly acute PAs.
The purpose of this study was to assess in a large dataset the prevalence of acute PAs among patients with psoriasis seeking emergency dental treatment at the hospital and to assess the prevalence after adjusting for related systemic, behavioral, and treatment-related confounders.
All the procedures performed in our study followed the ethical standards of the Institutional Review Board (IRB) of the University of Florida (UF) and privacy rules for research on IRB approved de-identified data sets (approval date: April 6, 2021).
De-identified clinical data, extracted from the integrated i2b2 open-source platform provided by the UF Health Office of the Chief Data Officer, were analyzed from October 2016 through October 2025. The i2b2 platform enables querying large sets of clinical and genomic data.
Data from 2,108,676 patients visiting the UF Health Center were collected via queries on the National Institutes of Health- and UF-supported i2b2 platform. Patient diagnoses were standardized using International Classification of Diseases, 10th Revision (ICD-10) codes. The analysis included a heterogeneous patient population with diverse conditions, including cases of acute paranasal pathology without sinus involvement. All cases of acute PAs admitted to the urgent care clinic were diagnosed and coded with appropriate ICD codes by calibrated, experienced oral healthcare professionals.
Inclusion criteria encompassed all patients with the corresponding code for acute PAs without sinus (ICD-10: K04.7), whether treated or not treated endodontically, and psoriasis (ICD-10: L40). Patient records were digitized, and specific diagnoses of acute PAs and psoriasis in the total hospital population were identified using the appropriate ICD-10 codes. The dataset reflected encounter-level data, and repeated encounters for the same patient were merged to avoid duplication. The dataset also reflected unique individuals, and psoriasis diagnosis preceded acute PAs diagnosis in all cases. The dental caries index was not assessed since patients were seen for emergency dental treatment. If the natural tooth was salvageable, treatment included endodontic treatment and coronal restoration.
The odds ratios (ORs) for the prevalence of acute PAs and their association with psoriasis were evaluated with 95% confidence intervals, and the statistical difference between psoriasis patients and non-psoriasis patients was assessed using MEDCALC software (ver. 23.3.7; MedCalc Software Ltd, Ostend, Belgium). A standard normal deviation (z-value) was calculated as follows: ln(OR)/SE[ln(OR)] [27]. The p-value was defined as the two-tailed area under the normal distribution curve outside the ± z thresholds, with p < 0.05 indicating statistical significance. Sensitivity analyses were evaluated to test the robustness of findings.
Logistic regression was conducted for diabetes (ICD-10: E08–E13), nicotine dependence (ICD-10: Z72.0), and alcohol-related disorders (ARD) (ICD-10: F10) comorbidities, as well as biologic drug use (ICD-10: Z79.620), using the aggregated counts as weights in the model. Biologic drugs included adalimumab, etanercept, ustekinumab, secukinumab, and risankizumab. Biologic drug therapy was analyzed as a binary variable without differentiation by drug class, dose, or duration. Adjustments to such factors were made.
Of the 16,084 psoriasis patients, 224 also had acute PAs (Table 1). Females were more affected than males by a factor of 2. Whites were more affected than African Americans, more than fivefold, and other ethnicities, more than sevenfold (Table 1).
The OR for acute PAs in patients with psoriasis was 2.21 (Table 2). The difference in prevalence compared to the total hospital patient population was statistically significant (p < 0.0001).
After adjustment for diabetes comorbidity, the OR for acute PAs was 1.4, and the difference in prevalence compared with the total hospital patient population was statistically significant (p < 0.0001) (Table 3).
After adjustment for nicotine dependence comorbidity, the OR for acute PAs was 1.31, and the difference in prevalence as compared to the total hospital patient population was statistically significant (p < 0.01) (Table 3).
After adjustment for ARD comorbidity, the OR for acute PAs was 1.89, and the difference in prevalence as compared to the total hospital patient population was statistically significant (p < 0.001) (Table 3).
After adjustment for biologic drug use, the OR for acute PAs was 1.77, and the difference in prevalence compared to the total hospital patient population was statistically significant (p < 0.0001) (Table 3).
This large, real-world dataset from a hospital-based study (>2 million records) provides robust evidence of a significant association between psoriasis and acute PAs. It shows that individuals with psoriasis are more than twice as likely to experience acute PAs as the general hospital population. This strong association suggests that psoriasis may influence susceptibility to endodontic infections beyond risk factors such as dental caries and periodontal disease [26]. These data are consistent with previous studies of smaller cohorts, which confirm an association between psoriasis and apical inflammation [26,28].
The demographic distribution shows interesting patterns. Female patients with psoriasis were twice as likely as males to present with acute PAs. This increased risk may be explained by sex-specific immunological and hormonal factors that modulate both oral and systemic inflammation. Female sex is associated with distinct immune responses, including a generally heightened innate and adaptive immune reactivity [29]. Women exhibit increased production of proinflammatory cytokines (such as interleukin [IL]-6 and tumor necrosis factor [TNF]-α), which are central to both psoriasis pathogenesis and the progression of periapical disease [29,30]. The heightened inflammatory milieu may hypothetically accelerate the transition from chronic inflammation to acute abscess formation in patients with psoriasis. Prevalent among women with psoriasis, low vitamin D levels further compromise immune regulation and bone density, increasing susceptibility to oral infections and the development of acute PAs [31]. Nevertheless, the differences between female and male patients may also reflect access to healthcare, utilization patterns, or coding practices rather than biological susceptibility alone.
White patients constituted the vast majority of psoriatic individuals with PAs (>75%). This proportion is notably higher than their representation in either the total psoriasis cohort or the overall acute PAs population. In contrast, African American patients accounted for less than 40% of all acute PAs cases hospital-wide, but only exhibited circa 15% acute PAs among individuals with psoriasis. These discrepancies cannot be explained by the demographic distribution of acute PAs in the overall hospital population. Therefore, it may suggest that psoriasis can act as a disease-specific modifier for increased risk of acute PAs. Differences in oral health behaviors, access to dental care, systemic inflammatory burden, or patterns of healthcare utilization across demographic groups may contribute to this phenomenon.
An important component of this study was the evaluation of whether the association between psoriasis and acute PAs could be attributed to comorbid conditions known to increase the risk of oral and periapical infections [26,32,33]. After adjustment for diabetes, a well-established risk factor [34], the OR decreased but remained highly significant. This decrease indicates that, while diabetes partially explains the increased risk of acute PAs in psoriatic patients, psoriasis retains an independent effect. A similar pattern emerged after controlling for nicotine dependence, underscoring that smoking contributes to, but does not fully account for, the elevated risk [35]. Furthermore, adjustment for ARD produced an OR slightly lower than the unadjusted estimate. It suggests that alcohol consumption, although associated with poor oral hygiene and impaired immune function, is not a major confounder in the psoriasis-acute PAs relationship. Psoriasis itself remains a dominant contributor to infection susceptibility even after accounting for this behavioral risk factor.
Particularly noteworthy is the persistence of a significant association after adjustment for biologic therapy. Biologic agents affect cytokine pathways that are essential to both psoriasis pathogenesis and host defense mechanisms [26]. Patients receiving biologic drugs typically present with more severe or refractory psoriasis. The use of such drugs is likely to act as a proxy for severe or refractory psoriasis. The elevated risk for acute PAs in this subgroup may reflect the systemic inflammatory burden of severe disease rather than a medication effect.
Additionally, since psoriasis severity could not be assessed in this de-identified dataset, biologic therapy may serve as a marker of more severe or refractory disease rather than indicating a direct medication-related effect. Moreover, biologic therapies were analyzed as a single category, precluding assessment of class-specific differences. Taken together, these findings suggest that while biologic therapy may be associated with reduced chronic periapical inflammatory severity [26], patients with more severe psoriasis may remain vulnerable to acute PAs. This observation likely reflects the combined influence of underlying disease severity, systemic inflammatory burden, and immune modulation, rather than a causal effect of biologic agents alone. Studies incorporating validated psoriasis severity scores will aid in understanding medication-related susceptibility in the context of disease-driven vulnerability.
Shared inflammatory pathways support the biological plausibility of an association between psoriasis and acute PAs. Cytokines such as IL-17 and TNF-α, key components of psoriasis immunopathogenesis, are also central mediators in apical inflammation, contributing to bone resorption and tissue destruction [26,36]. Systemic inflammation characteristic of psoriasis may impair host responses to pulpal infection, thereby accelerating the progression from pulp necrosis to abscess formation. Additionally, behavioral and psychosocial factors often linked to psoriasis, including depression, stress, and decreased oral healthcare engagement, may further contribute to delayed detection and increased emergency treatment needs [36].
The novel contribution of this study using a very large hospital dataset enabled robust statistical comparisons and enhanced generalizability within similar healthcare settings. The use of ICD-10–coded diagnoses by trained oral health professionals supports the accuracy of case classification [37]. However, some limitations must be acknowledged. First, the use of de-identified retrospective data limits the ability to assess clinical confounders such as caries index, periodontal status, oral hygiene status, socioeconomic background, dental visit frequency, or severity of psoriasis. Second, causality cannot be inferred from these cross-sectional observational data. Third, this study used a database from a single medical institution in the United States. Socioeconomic factors may affect certain populations' decisions to seek medical and dental care at this specific health center.
Fourth, potential heterogeneities and misclassification inherent to ICD-based diagnoses may limit the ability to assess psoriasis severity scores, disease duration, or flare-up status. Fifth, biologic therapy was analyzed only as a grouped category; individual drug effects might differ. Finally, emergency department-based identification of acute PAs may underestimate the number of less severe cases managed in outpatient dental clinics. Despite these limitations, the findings support an independent association between psoriasis and acute PAs.
The findings of this study highlight the importance of increased dental surveillance in psoriasis patients, particularly among those with behavioral risk factors or undergoing biologic therapy. An interdisciplinary collaboration between dermatology and dental care to establish early diagnosis and preventive treatment is encouraged. It should include frequent consultation and medication review, increased recall dental visits, a comprehensive oral exam, and patient education emphasizing rigorous oral hygiene.
In conclusion, psoriasis is independently associated with a higher prevalence of acute PAs, even after adjustment for systemic, behavioral, and treatment-related confounders. This association suggests that systemic inflammation and immune dysregulation may increase susceptibility to acute PAs. Future research should focus on prospective clinical studies that incorporate standardized assessments of psoriasis severity, detailed endodontic clinical evaluations, and stratification by specific biologic therapies to clarify how systemic inflammation and immunomodulatory treatment influence the risk and presentation of odontogenic and endodontic infections.

CONFLICT OF INTEREST

No potential conflict of interest relevant to this article was reported.

FUNDING/SUPPORT

The authors have no financial relationships relevant to this article to disclose.

AUTHOR CONTRIBUTIONS

Conceptualization: Rotstein I, Garcia-Godoy F. Investigation, Methodology: Rotstein I, Katz J. Writing - original draft: Rotstein I. Writing - review & editing: Grandini S, Malvicini G, Garcia-Godoy F. All authors read and approved the final manuscript.

DATA SHARING STATEMENT

The datasets are available from the corresponding author upon reasonable request.

DISCLOSURE OF GENERATIVE AI IN SCIENTIFIC WRITING

No generative AI tools were used in the preparation of this manuscript.

Table 1.
Demographic distribution of acute PAs and psoriasis patients among the total hospital population (n = 2,108,676)
Characteristic Psoriasis patients with acute PAs Total psoriasis patients Total acute PAs
No. of patients 224 16,084 13,473
Sex
 Female 146 (65.2) 9,434 (58.7) 7,543 (56.0)
 Male 78 (34.8) 6,650 (41.4) 5,930 (44.0)
Race/ethnicity
 African American 32 (14.3) 989 (6.2) 4,847 (36.0)
 White 172 (76.8) 10,269 (63.9) 7,437 (55.2)
 Other 20 (8.9) 4,826 (30.0) 1189 (8.8)
Age (yr)
 <18 10 (4.5) 569 (3.5) 1,650 (12.3)
 ≥18 214 (95.5) 15,515 (96.5) 11,823 (87.8)

Values are presented as number or number (%).

PA, periapical abscess.

Table 2.
Association between psoriasis and acute PAs in hospital patients
Variable PAs No PAs Odds ratio (95% CI) p-value
Psoriasis 224 15,860 2.21 (1.94–2.53) <0.0001
No psoriasis 13,247 2,079,345 1.00 (Reference) -

CI, confidence interval; PA, periapical abscess.

Table 3.
Association between psoriasis and acute PAs after adjustment for diabetes, nicotine dependence, ARD, and biologic drug use
Adjustment Psoriasis (PAs) No psoriasis (PAs) Odds ratio (95% CI) p-value
Diabetes 143 13,328 1.40 (1.18–1.65) <0.0001
Nicotine dependence 134 13,337 1.31 (1.10–1.55) <0.01
ARD 194 13,277 1.89 (1.64–2.18) <0.0001
Biologic drug use 181 13,290 1.77 (1.53–2.05) <0.0001

ARD, alcohol-related disorders; CI, confidence interval; PA, periapical abscess.

  • 1. Griffiths CE, Armstrong AW, Gudjonsson JE, Barker JN. Psoriasis. Lancet 2021;397:1301-1315.ArticlePubMed
  • 2. Michalek IM, Loring B, John SM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol 2017;31:205-212.ArticlePubMedPDF
  • 3. Brezinski EA, Dhillon JS, Armstrong AW. Economic burden of psoriasis in the United States: a systematic review. JAMA Dermatol 2015;151:651-658.ArticlePubMed
  • 4. Zhou S, Yao Z. Roles of infection in psoriasis. Int J Mol Sci 2022;23:6955.ArticlePubMedPMC
  • 5. Rousset L, Halioua B. Stress and psoriasis. Int J Dermatol 2018;57:1165-1172.ArticlePubMedPDF
  • 6. Nicholas MN, Gooderham M. Psoriasis, depression, and suicidality. Skin Therapy Lett 2017;22:1-4.
  • 7. Yaffee HS. Trauma and pustular psoriasis. J Am Acad Dermatol 1985;13:1055-1057.Article
  • 8. Pezzolo E, Naldi L. The relationship between smoking, psoriasis and psoriatic arthritis. Expert Rev Clin Immunol 2019;15:41-48.ArticlePubMed
  • 9. Kunz M, Simon JC, Saalbach A. Psoriasis: obesity and fatty acids. Front Immunol 2019;10:1807.ArticlePubMedPMC
  • 10. Wei J, Zhu J, Xu H, Zhou D, Elder JT, Tsoi LC, et al. Alcohol consumption and smoking in relation to psoriasis: a Mendelian randomization study. Br J Dermatol 2022;187:684-691.ArticlePubMedPDF
  • 11. Takeshita J, Grewal S, Langan SM, Mehta NN, Ogdie A, Van Voorhees AS, et al. Psoriasis and comorbid diseases: epidemiology. J Am Acad Dermatol 2017;76:377-390.ArticlePubMedPMC
  • 12. Mamizadeh M, Tardeh Z, Azami M. The association between psoriasis and diabetes mellitus: a systematic review and meta-analysis. Diabetes Metab Syndr 2019;13:1405-1412.ArticlePubMed
  • 13. Rendon A, Schäkel K. Psoriasis pathogenesis and treatment. Int J Mol Sci 2019;20:1475.ArticlePubMedPMC
  • 14. Schleicher SM. Psoriasis: pathogenesis, assessment, and therapeutic update. Clin Podiatr Med Surg 2016;33:355-366.ArticlePubMed
  • 15. Liang Y, Sarkar MK, Tsoi LC, Gudjonsson JE. Psoriasis: a mixed autoimmune and autoinflammatory disease. Curr Opin Immunol 2017;49:1-8.ArticlePubMedPMC
  • 16. Johnston A, Xing X, Wolterink L, Barnes DH, Yin Z, Reingold L, et al. IL-1 and IL-36 are dominant cytokines in generalized pustular psoriasis. J Allergy Clin Immunol 2017;140:109-120.ArticlePubMed
  • 17. Dupire G, Droitcourt C, Hughes C, Le Cleach L. Antistreptococcal interventions for guttate and chronic plaque psoriasis. Cochrane Database Syst Rev 2019;3:CD011571.ArticlePubMedPMC
  • 18. Nalliah RP, Allareddy V, Elangovan S, Karimbux N, Lee MK, Gajendrareddy P, et al. Hospital emergency department visits attributed to pulpal and periapical disease in the United States in 2006. J Endod 2011;37:6-9.ArticlePubMed
  • 19. Shah AC, Leong KK, Lee MK, Allareddy V. Outcomes of hospitalizations attributed to periapical abscess from 2000 to 2008: a longitudinal trend analysis. J Endod 2013;39:1104-1110.ArticlePubMed
  • 20. Brooks JK. Psoriasis: a review of systemic comorbidities and dental management considerations. Quintessence Int 2018;49:209-217.ArticlePubMed
  • 21. Kwak EJ, Choi YJ, Kim HN, Kim KE, Jeon J, Baek YS. Increased dental comorbidities in patients with psoriasis: a nationwide population-based cohort study in Korea. Clin Exp Dermatol 2023;48:1347-1353.ArticlePubMedPDF
  • 22. Ungprasert P, Wijarnpreecha K, Wetter DA. Periodontitis and risk of psoriasis: a systematic review and meta-analysis. J Eur Acad Dermatol Venereol 2017;31:857-862.ArticlePubMedPDF
  • 23. Nijakowski K, Gruszczyński D, Kolasińska J, Kopała D, Surdacka A. Periodontal disease in patients with psoriasis: a systematic review. Int J Environ Res Public Health 2022;19:11302.ArticlePubMedPMC
  • 24. Lazaridou E, Tsikrikoni A, Fotiadou C, Kyrmanidou E, Vakirlis E, Giannopoulou C, et al. Association of chronic plaque psoriasis and severe periodontitis: a hospital based case-control study. J Eur Acad Dermatol Venereol 2013;27:967-972.ArticlePubMed
  • 25. Sharma A, Raman A, Pradeep AR. Association of chronic periodontitis and psoriasis: periodontal status with severity of psoriasis. Oral Dis 2015;21:314-319.ArticlePubMed
  • 26. Marruganti C, Malvicini G, Cinotti E, Fuso A, Trovato E, Rubegni P, et al. Association between apical periodontitis and psoriasis vulgaris: a cross-sectional study. Int Endod J 2025;58:848-861.ArticlePubMedPMC
  • 27. Sheskin DJ. Handbook of parametric and nonparametric statistical procedures; 5th ed. Boca Raton, FL: Chapman & Hall/CRC; 2011. p. 761-804.
  • 28. Allihaibi M, Niazi SA, Farzadi S, Austin R, Ideo F, Cotti E, et al. Prevalence of apical periodontitis in patients with autoimmune diseases: a case-control study. Int Endod J 2023;56:573-583.ArticlePubMedPDF
  • 29. Bartz D, Chitnis T, Kaiser UB, Rich-Edwards JW, Rexrode KM, Pennell PB, et al. Clinical advances in sex- and gender-informed medicine to improve the health of all: a review. JAMA Intern Med 2020;180:574-583.ArticlePubMed
  • 30. Kouris A, Pistiki A, Katoulis A, Georgitsi M, Giatrakou S, Papadavid E, et al. Proinflammatory cytokine responses in patients with psoriasis. Eur Cytokine Netw 2014;25:63-68.ArticlePubMed
  • 31. Solak B, Dikicier BS, Celik HD, Erdem T. Bone mineral density, 25-OH vitamin D and inflammation in patients with psoriasis. Photodermatol Photoimmunol Photomed 2016;32:153-160.ArticlePubMed
  • 32. Malvicini G, Marruganti C, Abu Leil M, Martignoni M, Pasqui E, de Donato G, et al. Association between apical periodontitis and secondary outcomes of atherosclerotic cardiovascular disease: a case-control study. Int Endod J 2024;57:281-296.Article
  • 33. Gaeta C, Malvicini G, Di Lascio D, Martignoni M, Ragucci G, Grandini S, et al. Lifestyle, caries, and apical periodontitis: results from a university-based cross-sectional study. Int Endod J 2025;58:257-272.ArticlePubMed
  • 34. Pérez-Losada FL, Estrugo-Devesa A, Castellanos-Cosano L, Segura-Egea JJ, López-López J, Velasco-Ortega E. Apical periodontitis and diabetes mellitus type 2: a systematic review and meta-analysis. J Clin Med 2020;9:540.ArticlePubMed
  • 35. Pinto KP, Ferreira CM, Maia LC, Sassone LM, Fidalgo TK, Silva EJ. Does tobacco smoking predispose to apical periodontitis and endodontic treatment need?: a systematic review and meta-analysis. Int Endod J 2020;53:1068-1083.ArticlePubMedPDF
  • 36. do Nascimento TA, Verner FS, Lemos CA, Junqueira RB. Association between apical periodontitis and autoimmune diseases: a systematic review with meta-analysis. J Endod 2025;51:562-570.ArticlePubMed
  • 37. Figueiredo RL, Singhal S, Dempster L, Hwang SW, Quinonez C. The accuracy of international classification of diseases coding for dental problems not associated with trauma in a hospital emergency department. J Public Health Dent 2015;75:343-347.ArticlePubMedPDF

Tables & Figures

REFERENCES

    Citations

    Citations to this article as recorded by  

      • ePub LinkePub Link
      • Cite
        CITE
        export Copy Download
        Close
        Download Citation
        Download a citation file in RIS format that can be imported by all major citation management software, including EndNote, ProCite, RefWorks, and Reference Manager.

        Format:
        • RIS — For EndNote, ProCite, RefWorks, and most other reference management software
        • BibTeX — For JabRef, BibDesk, and other BibTeX-specific software
        Include:
        • Citation for the content below
        Prevalence of periapical abscesses in psoriasis patients: a retrospective cross-sectional study
        J Korean Acad Conserv Dent. ;e39  Published online August 10, 2026
        Close
      • XML DownloadXML Download
      Related articles
      Prevalence of periapical abscesses in psoriasis patients: a retrospective cross-sectional study
      Prevalence of periapical abscesses in psoriasis patients: a retrospective cross-sectional study
      Characteristic Psoriasis patients with acute PAs Total psoriasis patients Total acute PAs
      No. of patients 224 16,084 13,473
      Sex
       Female 146 (65.2) 9,434 (58.7) 7,543 (56.0)
       Male 78 (34.8) 6,650 (41.4) 5,930 (44.0)
      Race/ethnicity
       African American 32 (14.3) 989 (6.2) 4,847 (36.0)
       White 172 (76.8) 10,269 (63.9) 7,437 (55.2)
       Other 20 (8.9) 4,826 (30.0) 1189 (8.8)
      Age (yr)
       <18 10 (4.5) 569 (3.5) 1,650 (12.3)
       ≥18 214 (95.5) 15,515 (96.5) 11,823 (87.8)
      Variable PAs No PAs Odds ratio (95% CI) p-value
      Psoriasis 224 15,860 2.21 (1.94–2.53) <0.0001
      No psoriasis 13,247 2,079,345 1.00 (Reference) -
      Adjustment Psoriasis (PAs) No psoriasis (PAs) Odds ratio (95% CI) p-value
      Diabetes 143 13,328 1.40 (1.18–1.65) <0.0001
      Nicotine dependence 134 13,337 1.31 (1.10–1.55) <0.01
      ARD 194 13,277 1.89 (1.64–2.18) <0.0001
      Biologic drug use 181 13,290 1.77 (1.53–2.05) <0.0001
      Table 1. Demographic distribution of acute PAs and psoriasis patients among the total hospital population (n = 2,108,676)

      Values are presented as number or number (%).

      PA, periapical abscess.

      Table 2. Association between psoriasis and acute PAs in hospital patients

      CI, confidence interval; PA, periapical abscess.

      Table 3. Association between psoriasis and acute PAs after adjustment for diabetes, nicotine dependence, ARD, and biologic drug use

      ARD, alcohol-related disorders; CI, confidence interval; PA, periapical abscess.


      Restor Dent Endod : Restorative Dentistry & Endodontics
      Close layer
      TOP