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Article

Hyperuricemia as a Systemic Risk Factor for Periodontal Disease: A Review of Clinical and Microbial Evidence

by
Anca Silvia Dumitriu
1,
Stana Paunica
1,*,
Irina Bodnar
1,
Dragos Nicolae Ciongaru
1,
Brindusa Florina Mocanu
1,
Marina Cristina Giurgiu
1,
George Alexandru Denis Popescu
2 and
Dana Bodnar
3
1
Department of Periodontology, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania
2
Doctoral School, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania
3
Department of Restorative Odontotherapy, Faculty of Dental Medicine, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania
*
Author to whom correspondence should be addressed.
J. Mind Med. Sci. 2025, 12(1), 32; https://doi.org/10.3390/jmms12010032
Submission received: 16 February 2025 / Revised: 9 April 2025 / Accepted: 5 May 2025 / Published: 8 May 2025
Review Reports Versions Notes

Abstract

:
(1) Background: Hyperuricemia and periodontal disease are interconnected through shared inflammatory pathways, oxidative stress, and microbiome alterations. Both conditions involve chronic inflammation with uric acid contributing to systemic inflammation and oxidative stress that can exacerbate gum disease. Studies suggest that hyperuricemia may alter the oral microbiome, increasing the risk of periodontal infections. In addition, gout, a condition linked to chronic hyperuricemia, is associated with a higher prevalence of periodontal disease. (2) Objective: This study aims to investigate the association between hyperuricemia and periodontal disease, focusing on their inflammatory and microbial pathways. By integrating the literature data, the research attempts to better understand the potential role of gout as a risk factor for periodontal disease. (3) Methods: A systematic review was conducted following the PICOS framework, including studies that evaluated the association between gout and periodontal disease. (4) Results: The review highlighted a consistent association between gout and increased periodontal inflammation, which was likely driven by shared inflammatory mediators. (5) Conclusions: The effective management of periodontal disease in patients with gout requires supportive oral hygiene practices, lifestyle changes/control of uric acid levels through diet, as well as specific therapy to reduce inflammation and microbial pathogens to reduce disease severity.

1. Introduction

Periodontal disease and hyperuricemia, despite originating from distinct medical specialties, exhibit several links that have attracted growing interest in recent studies [1,2]. These two conditions, marked by chronic inflammation and systemic effects, highlight the complex relationship between oral health and overall well-being. Exploring this correlation not only deepens our understanding of their shared pathophysiology but also emphasizes the need for an integrative approach to diagnosis and treatment management.

1.1. Periodontal Disease

Periodontal disease, commonly referred to as periodontitis, is a chronic inflammatory condition that affects the supporting structures of the teeth, including the gingiva, periodontal ligament, cementum, and alveolar bone. It is primarily driven by a dysbiotic microbial matrix [3,4,5]. The host’s immune response to this biofilm triggers a chain of inflammatory processes, leading to progressive tissue destruction and eventual tooth loss if untreated. Periodontal disease has been identified as a significant public health issue, with a prevalence of 45–50% among adults globally, and it is linked to systemic conditions such as diabetes mellitus, cardiovascular diseases, and inflammatory arthritis [6]. Its chronic nature and systemic implications highlight its role as a potential contributor to inflammatory burdens across the body.

1.2. Gout Disease

Gout is a form of inflammatory arthritis caused by hyperuricemia or elevated levels of uric acid in the bloodstream. This metabolic imbalance results in the deposition of monosodium urate crystals within synovial joints, periarticular tissues, and sometimes visceral organs, triggering acute and painful inflammatory occurrences [2,7,8,9]. These episodes are often accompanied by skin rashes, swelling, and significant tenderness in the affected joints, the first metatarsophalangeal joint being the most frequently involved site. Beyond acute flares, chronic untreated gout can lead to the formation of monosodium urate (MSU) crystals surrounded by granulomatous tissue [10]. The condition is strongly influenced by genetic factors, dietary habits, and lifestyle choices, including the overconsumption of purine-rich foods and alcohol use [11]. Gout’s systemic nature has positioned it as a metabolic disorder with far-reaching health implications.

1.3. Linking Periodontal Disease and Gout

Periodontal disease and gout differ in their primary sites of manifestation—oral mucosa and alveolar bone versus joints. Despite that, they share overlapping mechanisms, such as chronic inflammation and intense host immune reaction. Research has begun to unravel potential pathways linking these conditions, such as systemic inflammation markers, oxidative stress, and unusual purine metabolism [12]. Understanding this connection is critical for recognizing oral health as a window to systemic health and for adopting a multidisciplinary approach to patient care.
Although these two conditions appear to belong to distinct medical domains, recent research suggests a strong link between periodontal disease and gout. Chronic inflammation and immune dysfunction seem to be the central elements connecting these conditions, offering an intriguing perspective on how oral health can influence or reflect the general health status [13,14,15].

2. Materials and Methods

This review aims to explore the association between hyperuricemia as a risk factor and periodontal disease, integrating findings from the literature. This systematic review was conducted using the PICOS (Population, Intervention, Comparison, Outcomes, Study design) framework to address the following clinical question: “In adults with hyperuricemia (P), does the presence and management of periodontal disease (I), compared to individuals without periodontal disease or receiving minimal treatment (C), influence the severity of periodontal inflammation, subgingival microbial dysbiosis, and systemic inflammatory markers (O)”? An exhaustive search was performed in databases including PubMed, Scopus, and Cochrane Library, targeting articles published between 2009 and 2024. Keywords used included “hyperuricemia”, “periodontal disease”, “systemic inflammation”, “microbial dysbiosis”, “clinical studies”, and “risk factors”. The initial search yielded a substantial number of articles exploring the relationship between hyperuricemia and periodontal disease.

2.1. Inclusion Criteria

Inclusion criteria were defined to select studies that met the focus and quality standards of this review. To be included, studies had to directly examine or discuss the potential links between periodontal disease and gout. Longitudinal studies and investigations discussing mechanisms, clinical associations, and microbiological findings were also considered. Other study criteria included the following: (1) patients diagnosed with periodontal disease according to criteria established by oral health and periodontal organizations; (2) patients receiving dental assessment and treatment for periodontal disease; (3) patients assessed for the presence and severity gout; (4) age range (18–80 years); (5) patients who can perform oral hygiene adequately according to the provided instructions (or their caregivers).

2.2. Exclusion Criteria

Exclusion criteria were applied to eliminate studies that did not contribute to the understanding of the connection between the two conditions and included the following: (1) studies not involving patients with hyperuricemia or periodontal disease, (2) non-peer-reviewed articles, reviews, or editorials without primary data, (3) insufficient clinical or microbiological data related to the research question, (4) interventions unrelated to periodontal disease management in gout patients, (5) articles not in English or published before 2009, (6) duplicate studies or overlapping data without additional insights.

2.3. Study Selection

Following the application of the inclusion and exclusion criteria, a refined selection of articles was identified for detailed analysis. Full-text versions of the selected studies were retrieved and reviewed (Table 1). Data extraction was conducted systematically including study title, publication year, study design (e.g., clinical trial, observational study, experimental study), primary focus (sample characteristics, mechanisms, clinical associations, microbiological findings, genetic correlations), and key outcomes (discussion, results and conclusions).

3. Results

The reviewed studies highlight a clear connection between periodontal disease and gout that is mediated by inflammation, serum uric acid levels, salivary metabolites, and periodontal pathogens. The interaction of these biological factors underscores the importance of a holistic approach in managing both conditions.
Chronic inflammation is a common link between periodontal disease and gout, serving as a key mechanism in the pathogenesis of both conditions. Studies have shown that hyperuricemia (elevated serum uric acid levels) contributes to systemic inflammation by stimulating pro-inflammatory pathways such as Toll-like receptor (TLR) activation and the release of cytokines (IL-1, IL-6, TNF-α) [8,12]. These inflammatory mechanisms exacerbate periodontal destruction by promoting bone resorption and damage to the supporting structures of the teeth. Furthermore, Chen et al. [18] in a study suggest that periodontal inflammation can elevate systemic inflammatory cytokine levels, exacerbating gout by increasing urate crystal deposition in joints. This creates a vicious cycle in which periodontal inflammation worsens gout. Meta-analyses [12,19] revealed that patients with high uric acid levels have an increased prevalence of periodontal disease. Uric acid plays a dual role in the body: it has antioxidant properties, but in excess, it can induce oxidative stress and chronic inflammation. In the context of periodontal disease, elevated uric acid levels may disrupt the metabolic homeostasis of oral tissues, contributing to periodontal structure breakdown [18,19,23].
Chen et al. [18] suggest that hyperuricemia can also alter saliva composition, creating a favorable environment for the proliferation of pathogenic bacteria involved in periodontal disease. Therefore, monitoring and controlling serum uric acid levels may be crucial not only for preventing gout but also for maintaining oral health. Saliva is a valuable indicator of both systemic and oral health. Studies have shown that patients with periodontitis exhibit elevated levels of oxidative stress metabolites, including uric acid and superoxide dismutasa [18,19]. This indicates that periodontal inflammatory processes can influence systemic purine metabolism, which may contribute to gout progression. Moreover, Barnes et al. [10] found that purine degradation is accelerated in patients with periodontitis, suggesting a direct link between oral metabolic dysfunction and hyperuricemia. Therefore, analyzing salivary metabolites could become a non-invasive screening method for identifying patients at higher risk for gout and periodontal disease.
The oral microbiome plays a crucial role in maintaining oral health balance. Studies have demonstrated that gout patients have a distinct microbial profile compared to healthy individuals with an increased abundance of pathogenic bacteria such as Prevotella intermedia, Porphyromonas gingivalis, and Fusobacterium nucleatum [1,22]. These bacteria are involved in periodontal inflammation and have been associated with increased inflammatory cytokine levels and tissue destruction. Furthermore, Kim et al. [2] highlighted that oral microbiome dysbiosis can also affect gut microbiota, influencing uric acid metabolism and contributing to its accumulation in the body. This suggests that addressing oral dysbiosis may positively impact the uric acid level control [2].

4. Discussion

4.1. Periodontal Pathogen

The classification proposed by Socransky (1998) is a well-known system in oral microbiology that is used to group bacteria associated with periodontal disease based on their pathogenic behavior and their association with different stages of the disease [4]. Socransky identified several bacterial complexes, which are each named after a specific color. These colors reflect the role of the bacteria in periodontal health or disease: The purple complex includes bacteria considered less pathogenic, such as Actinomyces species, which are associated with periodontal health and the early colonization of the biofilm. The green complex comprises bacteria such as Capnocytophaga species, Aggregatibacter actinomycetemcomitans (serotype a), and Eikenella corrodens, which are linked to biofilm colonization and the transition toward a more inflammatory environment. The orange complex includes bacteria such as Fusobacterium nucleatum, Prevotella intermedia, Prevotella nigrescens, and Parvimonas micra. These species act as intermediaries between less pathogenic bacteria and those in the red complex [17,20]. The red complex consists of highly pathogenic bacteria, including Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola. This complex is strongly associated with severe periodontal disease, advanced inflammation, and the destruction of periodontal tissues [17,20]. This classification helps to understand the dynamics of the oral biofilm and provides an important guide for assessing periodontal risk and directing treatment [4,24].
The microbiological analysis results support the hypothesis that systemic conditions, such as gout, may significantly influence the microbial composition associated with periodontal disease. The detection of high-risk pathogens, including Porphyromonas gingivalis (Pg), Treponema denticola (Td), and Tannerella forsythia (Tf), indicates a severe periodontal infection that is often associated with systemic inflammation and immune dysregulation [5,25].

4.2. Inflammatory Response

Gout, a condition marked by chronic hyperuricemia and heightened inflammatory responses, has been implicated in the worsening of periodontal disease through the increased production of pro-inflammatory cytokines. These mediators create a favorable environment for the proliferation of periodontal pathogens, further accelerating tissue destruction and alveolar bone loss. Additionally, the oxidative stress and metabolic dysregulation linked to gout may enhance bacterial virulence, exacerbating periodontal attachment loss and disease progression [11,17,18]. The moderate bacterial loads observed in Eikenella corrodens (Ec) and Campylobacter rectus (Cr) suggest that microbial dysbiosis extends beyond the red complex bacteria, involving a broader range of pathogens potentially influenced by systemic inflammatory states. Likewise, the lower bacterial counts of Capnocytophaga species (Co, Cs, Cg) indicate that while these bacteria are present, they are unlikely to be primary contributors to disease progression in patients with systemic risk factors like gout [26,27,28]. These findings highlight the importance of an interdisciplinary approach in managing patients with both gout and periodontitis, emphasizing the need for systemic inflammation control alongside targeted periodontal therapy. Future research should further investigate the direct microbial interactions between urate metabolism and periodontal pathogens, aiming to clarify the bidirectional relationship between these two inflammatory conditions.
In addition to the aspects related to periodontal disease, it is important to discuss the aspects concerning the patient’s general conditions and medication. The patients present with a complex medical history characterized by multiple systemic conditions, which may contribute to the intricate relationship between general pathologies—particularly gout—and periodontal disease [29]. The diagnosis of severe hypertension, managed with angiotensin receptor antagonists candesartan and calcium channel blockers, indicates a persistent vascular burden that may play a critical role in the amplification of systemic inflammatory responses. This observation is consistent with emerging evidence highlighting the association between hypertension, endothelial dysfunction, and heightened pro-inflammatory states, which have been implicated in the pathophysiology of periodontal inflammation [30].
Of particular interest is the diagnosis of gout, for which the patients are under chronic treatment with allopurinol [31,32]. Given that hyperuricemia is associated with increased systemic inflammation, oxidative stress, and altered immune responses, the presence of gout may serve as a key link between metabolic dysregulation and periodontal pathology. Uric acid crystals can contribute to local and systemic inflammatory cascades, which are mechanisms that mirror those observed in periodontitis [31]. The shared inflammatory pathways suggest a bidirectional relationship, where chronic periodontal disease might exacerbate gout flares, while gout-associated inflammation may worsen periodontal tissue destruction. Therefore, it is important to highlight in this study the aspects related to general conditions and their medication. The medication prescribed by the cardiologist, particularly oral anticoagulants, antiplatelet agents, and calcium channel antagonists, may play a significant role in gingival changes.

4.3. Periodontal Treatment

In some cases, after scaling and debridement, gingival inflammation did not improve satisfactorily, so local antibiotics were added. Even if the microbiological analysis shows the presence of aggressive periodontal species from the red complex, systemic antibiotic therapy is not recommended considering the patient’s gout medication. There are side effects of the combination of allopurinol with systemic antibiotics, especially those from the penicillin or tetracycline classes, so their use was not recommended [33].
Anticoagulant therapy, while crucial for cardiovascular protection, may also modulate the bleeding risks and wound-healing potential in periodontal interventions [34,35]. It is important to mention and specify that the International Normalized Ratio (INR) had normal values; therefore, the bleeding was not caused by anticoagulant medication. As a result, it was not necessary to discontinue the medication for the initial periodontal treatment (scaling, debridement) [36]. Considering the interconnection between these conditions, the patient’s cases reinforces the necessity of a multidisciplinary approach in managing systemic diseases with inflammatory components, particularly in individuals with both gout and periodontal disease. Further research is warranted to elucidate the specific mechanistic pathways linking these conditions and to explore potential shared therapeutic strategies.
The study design and statistical framework acknowledge concerns regarding the need for a more robust statistical approach with the primary objective being the exploration of the potential association between hyperuricemia and periodontal disease through a systematic review and a clinical case study. While the clinical cases do not establish causation, it serves to illustrate the potential clinical implications of this association, and future research will include larger cohort analyses with statistical modeling to strengthen the evidence base. A fundamental limitation of the current study is the lack of statistical validation of findings, as systematic reviews provide qualitative rather than quantitative conclusions. Future iterations should employ meta-analytical techniques to synthesize data, allowing for effect size calculations, confidence intervals, and heterogeneity assessments.
Statistical evidence and claims require additional validation with the study aiming to enhance the discussion by incorporating more detailed statistical findings from the reviewed literature. Further studies incorporating larger cohorts and prospective longitudinal components will help establish temporal relationships between hyperuricemia and periodontal disease progression.
The studies included in the review reported significant associations between serum uric acid levels and periodontal disease severity, with findings such as a positive correlation between uric acid levels and clinical attachment loss, and an increased risk of severe periodontitis in individuals with elevated uric acid levels. Integrating such statistical data provides a stronger evidentiary basis for the proposed link between gout and periodontal disease with future studies needing to explore dose–response relationships and conduct multivariate analyses to control for confounding factors.
The association between gout and periodontal disease involves inflammatory pathways, metabolic dysregulation, and microbial dysbiosis, yet alternative explanations such as lifestyle factors including diet, smoking, and alcohol consumption must be considered. Many studies fail to adequately control for these variables, raising concerns regarding residual confounding.
Future research should explore the use of anti-inflammatory agents in periodontal therapy given the role of IL-1, TNF-α, and IL-6 in both conditions. Targeted biologic therapies and dietary modifications aimed at reducing systemic uric acid levels may offer adjunctive approaches to periodontal disease management. Also, research directions highlight the need for larger comparative studies, mechanistic research, and statistical validation to confirm findings. Key areas for future exploration include large interventional trials evaluating the impact of uric acid-lowering therapy on periodontal health, metagenomic and metabolomic studies characterizing microbial signatures associated with hyperuricemia and periodontitis, and systems biology approaches integrating multi-omics data to uncover shared pathogenic pathways. While the study provides preliminary insights into the link between gout and periodontal disease, significant research gaps remain, requiring rigorous methodological approaches to enhance understanding of the systemic interplay between metabolic and inflammatory disorders. The constructive feedback provided is appreciated, and necessary revisions will be made to enhance the scientific rigor of the study.

5. Conclusions

When multiple predisposing factors are present, especially systemic ones, it is very difficult to determine which has the greatest influence. Therefore, understanding the histopathological implications at the periodontal level for each condition, as well as the side effects of systemic medication, is crucial in therapeutic management. It has been demonstrated that plaque and calculus removal led to an improvement in periodontal status. However, the presence of aggressive periodontal pathogens in the context of tissue damage caused by systemic conditions such as diabetes, hypertension, and gout require more complex therapeutic approaches, including combinations of antiseptics and antibiotics, and, importantly, long-term patient monitoring protocols.
The clinical case studies demonstrated that targeted periodontal therapy in a patient with gout resulted in significant improvements across multiple clinical parameters. The reduction in inflammation, calculus index, bleeding, and probing depth underscores the efficacy of a comprehensive treatment plan that includes antimicrobial interventions and consistent oral hygiene practices. These findings highlight the importance of interdisciplinary management for patients with systemic conditions like gout, emphasizing the role of periodontal health in overall well-being.

Author Contributions

Conceptualization, A.S.D. and S.P.; methodology, I.B.; software, D.N.C.; validation, A.S.D., S.P. and M.C.G.; formal analysis, I.B.; investigation, D.N.C.; resources, B.F.M.; data curation, G.A.D.P.; writing—original draft preparation, I.B.; writing—review and editing, S.P.; visualization, D.B.; supervision, A.S.D.; project administration, B.F.M.; funding acquisition, M.C.G. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

The study was conducted according to the guidelines of the Declaration of Helsinki and approved by the Ethics Committee of the University of Medicine and Pharmacy Carol Davila, number 2945/14.02.2025.

Informed Consent Statement

Informed consent was obtained from all subjects involved in the study.

Data Availability Statement

Data are contained within the article.

Acknowledgments

All authors have accepted responsibility for the entire content of this manuscript approved its submission and have consented to the acknowledgement. Publication of this paper was supported by the University of Medicine and Pharmacy Carol Davila through the institutional program Publish not Perish.

Conflicts of Interest

The authors declare no conflicts of interest.

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Table 1. Hyperuricemia and periodontal disease studies.
Table 1. Hyperuricemia and periodontal disease studies.
Study (Author, Year)Number of CasesVariables InvestigatedType of StudyKey Findings
Inflammation
Chen et al. (2020) [7]Not specified Relationship between hyperuricemia and periodontitisHypothesis/theoretical studySuggests hyperuricemia may be a risk factor for periodontitis due to its effects on inflammation and oxidative stress
Hou et al. (2022) [8]Review (no original cases)Association between hyperuricemia and periodontitis (mechanisms, evidence from studies)Narrative reviewHighlights biological links: inflammation, oxidative stress, immune dysregulation. Suggests hyperuricemia may contribute to periodontitis progression
Uppin and Varghese (2023) [16]Systematic review (multiple studies included)Role of uric acid in oral and systemic healthSystematic reviewCompiles evidence linking uric acid to oral inflammatory conditions, including periodontitis; notes dual role—antioxidant and pro-inflammatory
Gradinaru et al. (2020) [17]Review/discussion (case-based)Oral manifestations of gout, metabolic disordersNarrative review/case-basedHighlights links between gout, hyperuricemia and oral lesions including possible periodontal impact in the context of metabolic syndrome
Chen et al. (2020) (Taiwan) [18]Large national population dataset (exact number not specified here)Gout as a risk factor for periodontal diseasePopulation-based cohort studyFound statistically significant association between gout and increased risk of developing periodontitis
Ye et al. (2023) [12]Systematic review and meta-analysis (include multiple studies)Uric acid levels in blood and oral fluids in relation to periodontitisSystematic review and meta-analysisSignificant association found: higher uric acid levels in individuals with periodontitis, especially in oral fluids; supports link between hyperuricemia and periodontal inflammation
Bai et al. (2024) [19]Not specified in the citation (likely a population sample)Serum uric acid levels and periodontitis statusCross-sectional studyFound a positive association between elevated serum uric acid and periodontitis; suggests uric acid may serve as a biomarker or modifiable risk factor
Salivary Metabolites
Tsai et al. (2021) [20]1123 participantsserum triglycerides, serum uric acid, plasma glucoseCase-control studyLinks metabolic biomarkers to periodontitis in young adults
Narendra et al. (2018) [21]46 patients with chronic periodontitis, 32 patients with aggressive periodontitis, and 50 healthy controlsspecific metabolites (lactate, acetates)ObservationalSuperoxide dismutase (SOD), nonenzymatic antioxidant uric acid, and lipid peroxidation suggests uric acid as a risk factor to periodontal disease
Barnes et al. (2009) [10]22 persons with chronic periodontitisreactive oxygen species (ROS) productionResearch reportsHighlights increased purine degradation in periodontal disease
Byun et al. (2020) [9]173,209 participants, 8809 with hyperuricemia and 126,465 controls (non-hyperuricemia)reactive oxygen species (ROS) productionA cross-sectional studyExamines hyperuricemia-periodontitis association in a large cohort study
Periodontal Pathogens
Yu et al. (2021) [22]N/AEscherichia coli, Fusobacterium nucleatum and Helicobacter pylorReviewGut microbiota influences the development of various diseases (e.g., metabolic, immune, neurological, cancer). Fecal microbiota transplantation (FMT) shows potential as a therapy
Kim et al. (2022) [2]60 patientsFirmicutes Bacteroidetes and Prevotella Bacteroides Cross-sectionalIdentifies distinct gut microbiota patterns in hyperuricemic patients
Liu et al. (2018) [1]23 gout patients, and 19 healthy control subjectsPrevotella IntermediaCase-control studyFinds increased abundance in gout patients, linking oral microbiota changes with systemic inflammation
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Dumitriu, A.S.; Paunica, S.; Bodnar, I.; Ciongaru, D.N.; Mocanu, B.F.; Giurgiu, M.C.; Popescu, G.A.D.; Bodnar, D. Hyperuricemia as a Systemic Risk Factor for Periodontal Disease: A Review of Clinical and Microbial Evidence. J. Mind Med. Sci. 2025, 12, 32. https://doi.org/10.3390/jmms12010032

AMA Style

Dumitriu AS, Paunica S, Bodnar I, Ciongaru DN, Mocanu BF, Giurgiu MC, Popescu GAD, Bodnar D. Hyperuricemia as a Systemic Risk Factor for Periodontal Disease: A Review of Clinical and Microbial Evidence. Journal of Mind and Medical Sciences. 2025; 12(1):32. https://doi.org/10.3390/jmms12010032

Chicago/Turabian Style

Dumitriu, Anca Silvia, Stana Paunica, Irina Bodnar, Dragos Nicolae Ciongaru, Brindusa Florina Mocanu, Marina Cristina Giurgiu, George Alexandru Denis Popescu, and Dana Bodnar. 2025. "Hyperuricemia as a Systemic Risk Factor for Periodontal Disease: A Review of Clinical and Microbial Evidence" Journal of Mind and Medical Sciences 12, no. 1: 32. https://doi.org/10.3390/jmms12010032

APA Style

Dumitriu, A. S., Paunica, S., Bodnar, I., Ciongaru, D. N., Mocanu, B. F., Giurgiu, M. C., Popescu, G. A. D., & Bodnar, D. (2025). Hyperuricemia as a Systemic Risk Factor for Periodontal Disease: A Review of Clinical and Microbial Evidence. Journal of Mind and Medical Sciences, 12(1), 32. https://doi.org/10.3390/jmms12010032

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