Bridging systems: oral-kidney connections - pathophysiological links, clinical implications, and health system integration – a narrative review

Abstract

Emerging evidence supports a bidirectional relationship between chronic kidney disease (CKD) and oral diseases, mediated by systemic inflammation, endothelial dysfunction, and immune dysregulation. Periodontitis and caries are prevalent yet underrecognized contributors to the inflammatory burden in CKD, particularly in low-resource settings where oral and kidney care remain fragmented. This reviewsynthesizes clinical, epidemiologic, and mechanistic evidence fromobservational studies, interventional trials, and meta-analyses examiningoral–renal interactions. PubMed-indexed literature was analyzed to map oralhealth indices, stage-specific manifestations, and the impact of periodontaltherapy on systemic biomarkers in CKD. Across multipleclinical studies, oral disease severity increases in parallel with CKDprogression and systemic inflammation. Elevated dental indices, includingdecayed, missing, and filled teeth (DMFT), plaque index, gingival index, andclinical attachment loss, correlate with reduced glomerular filtration rate andincreased inflammatory markers such as C-reactive protein and interleukin-6. Non-surgical periodontal therapy modestly improves inflammatory profiles,though renal outcomes remain variable. Post-transplant populations exhibitunique oral complications, including gingival overgrowth, candidiasis, andmucosal neoplasia, linked to immunosuppressive regimens. Oral healthconstitutes a measurable and modifiable determinant in CKD progression.Integrating oral assessments into nephrology care can enhance the monitoring ofsystemic inflammation and improve patient quality of life. Structuralinequities and limited workforce capacity continue to impede global oral–renalintegration. Evidence-based, interdisciplinary strategies are proposed to embedoral health within CKD management pathways.

Introduction

Chronic kidney disease (CKD) is a rapidly growing global cause of death and disability, projected to become a top cause of years of life lost by 2040 [1, 2]. The economic burden is substantial; in the United States alone, annual Medicare spending approaches $130 billion [3].

Oral diseases, especially periodontitis, interact with CKD through inflammatory and microbial pathways that extend beyond the mouth, positioning oral health as both a marker and mediator of systemic dysfunction [4]. Emerging evidence supports a bidirectional relationship between periodontitis and chronic kidney disease (CKD). Periodontal inflammation contributes to systemic cytokine elevation and endothelial dysfunction, potentially accelerating the decline in renal function, whereas uremia-associated immune dysregulation and impaired tissue repair exacerbate periodontal pathology [5, 6]. Dysbiosis of the oral microbiome contributes to systemic endotoxemia, leading to tubulointerstitial, glomerular, and vascular injury (endothelial dysfunction), which are central mechanisms in CKD progression [7]. CKD’s global burden is unevenly distributed: approximately 80% of affected individuals live in low- and middle-income countries (LMICs), where late diagnosis, under-resourced health systems, and limited preventive strategies accelerate disease progression [8–10].

Oral diseases collectively affect an estimated 3.7 billion individuals worldwide, accounting for a substantial share of the global disease burden [11]. According to the Global Burden of Disease Study 2021, untreated dental caries in permanent dentition remains the most prevalent condition globally [12]. Moreover, periodontal diseases affected approximately 951.3 million individuals in 2021, reflecting a persistent and significant global public health concern [13]. In the United States alone, annual expenditures on dental care are estimated at more than $136 billion, reflecting the substantial economic burden of oral diseases [14].

Periodontitis has emerged as a non-traditional yet modifiable risk factor influencing kidney outcomes [15, 16]. Clinical studies report that moderate‑to‑severe periodontitis correlates with accelerated glomerular filtration rate (GFR) decline and higher all-cause mortality among CKD patients [17–19]. Mechanistic research has linked periodontal inflammation to elevated systemic markers, such as C-reactive protein (CRP) and interleukin-6 (IL-6), which contribute to kidney fibrosis and cardiovascular morbidity [20–22]. However, most available data are observational with modest effect sizes, and many of the implicated inflammatory pathways are shared with other chronic conditions. Interventional studies reinforce this relationship, and meta-analyses of non-surgical periodontal therapy (NSPT) demonstrate modest improvements in estimated glomerular filtration rate (eGFR) and reductions in systemic inflammation among patients with CKD, suggesting that co-management of oral disease may attenuate deterioration in kidney function [23].

The convergence of these two high-prevalence conditions, chronic kidney disease and periodontitis, constitutes a dual global burden with far-reaching biological, clinical, and economic consequences. Yet, despite mounting evidence linking their shared pathophysiology, nephrology and oral health continue to operate as siloed disciplines, with limited translation of integrated insights into clinical practice or health policy [24–26]. Integrating standardized oral assessments into CKD risk stratification and earlier detection could complement existing screening approaches and potentially reduce systemic inflammation and improve quality of life. This review, therefore, synthesizes the biological, clinical, and systemic intersections between oral and kidney health, with particular attention to how oral findings may inform earlier CKD detection and risk stratification, and identifies research priorities and implementation opportunities to guide equitable, multidisciplinary care.

Pathophysiological mechanisms linking periodontitis to systemic disease (Figure 1)

Fig. 1.

Pathophysiological mechanisms linking periodontitis to systemic and kidney disease

The pathogenesis of periodontitis is multifactorial, involving complex interactions among the oral microbiome, host immune responses, and systemic vascular pathways.

Homeostasis and early disruption

In periodontal health, a symbiotic balance exists between commensal Gram-positive aerobes and neutrophils, which are engaged in immunosurveillance [26, 27]. Gingival crevicular fluid maintains this equilibrium by transporting complement proteins and immunoglobulins into the gingival crevice, enabling controlled microbial–immune interactions. Disruption of plaque homeostasis on the enamel surface activates epithelial Toll-like receptors, initiating nuclear factor κ-B (NF-κB) signaling and the release of pro-inflammatory mediators, including tumor necrosis factor (TNF), IL-1β, IL-8, and complement components [28]. The ensuing vasodilatation and increased vascular permeability facilitate neutrophil migration and gingival edema, marking the onset of gingivitis. When this inflammatory state becomes chronic, repeated bacteremia and sustained cytokine spillover into the systemic circulation amplify low-grade systemic inflammation, endothelial dysfunction, and oxidative stress, pathways increasingly implicated in the progression of chronic kidney disease [29]. Circulating periodontal pathogens and inflammatory mediators may directly injure glomerular and tubular cells or exacerbate pre-existing CKD by promoting immune activation, microvascular damage, and accelerated atherosclerosis, thereby linking periodontal inflammation to adverse kidney health outcomes [30].

Chronic inflammation and tissue destruction

Failure to resolve this acute response leads to chronic inflammation, characterized by TH17 and plasma cell infiltration. IL-17 and receptor-activator of NF-κB ligand (RANKL) signaling drive osteoclast activation, leading to alveolar bone resorption, while matrix metalloproteinases (MMPs) degrade collagen, promoting immune cell recruitment [31]. The inflamed microenvironment supports microbial dysbiosis, enriching pathogens such as Porphyromonas gingivalis and Fusobacterium nucleatum. This dysbiosis further amplifies inflammation, creating a self-sustaining pathogenic cycle [32]. Beyond the oral cavity, this persistent inflammatory burden and episodic translocation of periodontal pathogens contribute to systemic immune activation, skewing cytokine profiles toward a pro-inflammatory and pro-fibrotic state that may adversely affect renal microvasculature and tubular integrity [33]. Such chronic immune stimulation can exacerbate CKD by promoting endothelial dysfunction, accelerating renal fibrosis, and lowering the threshold for progressive kidney injury, thereby embedding periodontal disease within a broader systemic inflammatory network that includes the kidney [34].

Systemic immune activation

Ulceration of the periodontal pocket epithelium permits translocation of bacteria and host-derived mediators into circulation, triggering systemic complement activation, neutrophil priming, and oxidative stress. Periodontitis-induced systemic inflammation extends to the bone marrow, where hematopoietic stem cells undergo epigenetic reprogramming, producing hyper-reactive myeloid cells that perpetuate inflammation in distant organs [35]. In the kidney, this heightened innate immune tone may lower the threshold for injury by amplifying leukocyte recruitment, complement deposition, and oxidative damage within the glomerular and tubulointerstitial compartments [36]. Over time, such maladaptive immune activation can worsen renal inflammation, impair repair mechanisms, and accelerate CKD progression, providing a mechanistic bridge between periodontal immune dysregulation and sustained kidney injury [37].

Neutrophil dysfunction and end-organ effects

In established periodontitis, neutrophils exhibit delayed apoptosis, excessive production of reactive oxygen species (ROS), formation of neutrophil extracellular traps (NETs), and impaired chemotaxis [38]. These maladaptive responses propagate collateral tissue damage and autoimmunity. The resulting chronic systemic inflammation, characterized by elevated CRP, cytokinemia, and oxidative stress, links periodontitis to non-communicable diseases (NCDs) such as chronic kidney disease [39]. Within the kidney, heightened neutrophil activation and NET burden may promote endothelial injury, glomerular capillary damage, and tubulointerstitial inflammation, processes implicated in both CKD initiation and progression [40]. By fostering a pro-inflammatory and pro-thrombotic milieu, periodontitis-associated neutrophil dysfunction provides a biologically plausible pathway linking oral inflammation to progressive renal dysfunction and other non-communicable diseases [41].

Bidirectional pathophysiology: connecting biological systems (Figure 2)

Fig. 2.

Bidirectional relationship between chronic kidney disease and periodontal disease

The interaction between periodontal disease and CKD reflects a biologically plausible and clinically significant bidirectional relationship sustained by systemic inflammation, microbial dysbiosis, and immune dysregulation [42–44]. Accumulating evidence from systematic reviews, meta-analyses, and interventional trials underscores the mechanistic and clinical importance of oral–systemic pathways in CKD progression (Table 1).

Table 1.

Summary of clinical and observational studies on oral-systemic interactions in CKD

No	Author (Year)	Study design	Intervention	Outcome measures	Results	Principal conclusions
1	Ferreira et al [45].	Systematic Review and Meta-analysis	Periodontitis in CKD	CRP, hypoalbuminemia, CVD, all-cause mortality	PR = 2.47, PR = 1.35, RR = 2.29, RR = 1.73	Periodontitis linked to inflammation and mortality in CKD
2	Wu et al [46].	Systematic Review and Meta-analysis	Periodontitis (CAL-defined) in CKD	CVD, all-cause mortality	HR = 1.57 (CVD), HR = 1.24 (all-cause)	Periodontitis is a predictor of mortality in CKD
3	He et al [47].	Meta-analysis of Cohort Studies	Periodontitis in CKD	All-cause, cardiac mortality	RR = 1.32 (all-cause); RR = 1.31 (cardiac, sensitivity)	Periodontitis increases all-cause mortality; cardiac link probable
4	Church et al [48].	Systematic Review	Oral hygiene practices	Risk of T2DM, CVD, CKD, and mortality	Toothbrushing ↓ T2DM risk; ↓ CVD mortality; mouthwash ↑ risk	Oral hygiene protects against cardiometabolic diseases
5	He et al [21].	Umbrella Review	Existing SRs/MAs	Periodontitis–CKD directionality and treatment	18 SRs reviewed	Strong bidirectional relationship: clinical guidance proposed
6	Roberts et al [49].	Systematic Review and Meta-analysis	Periodontitis vs. healthy	Hb, RBC, Hct	Hb: g = −1.16; RBC: g = −0.85; Hct: g = −0.56	Periodontitis is associated with anemia
7	Chen & Li [22].	Systematic Review and Meta-analysis	Periodontitis and PT in ESKD	All-cause and CVD mortality	HR = 1.13 (NS); HR = 1.44 (CVD, NS); PT may help	No definitive mortality impact; PT potentially beneficial
8	Maheshwari et al [50].	Interventional Clinical Trial	NSPT in CKD (stages III–IV)	MDA, IL-1β, CRP	Inflammatory markers ↓ post-NSPT	NSPT may reduce systemic inflammation in CKD
9	Trzcionka et al [51].	Systematic Review	HD patients with DM/HTN	Periodontal status, mucosa, hygiene, candidiasis	Co-morbidities worsened oral health in HD	Multimorbidity worsens oral health outcomes
10	Bezerra et al [52].	Systematic Review and Meta-analysis	Periodontal treatment in HD patients	CRP levels	SMD = 0.45; p < 0.001; I2 = 0%	Periodontal therapy reduces CRP; low certainty evidence
11	Tavares et al [53].	Systematic Review	Periodontitis–CKD biomarkers	CRP, IL-6, NOx, etc.	Multiple inflammatory markers ↑ in PD–CKD	Supports the inflammatory burden hypothesis
12	Serni et al [54].	Systematic Review and Meta-analysis	CKD vs. Periodontitis	CAL, PPD, MH-OR	OR = 2.36; CAL ↑ 0.41 mm; PPD ↑ 0.25 mm	More severe CKD correlates with worse periodontal outcomes
13	Mahajan et al [54].	Systematic Review and Meta-analysis	Diabetes in HD patients	Periodontal status, salivary changes, oral manifestations	People with diabetes on HD had worse oral/periodontal outcomes	Diabetes worsens oral health in HD patients
14	Yue et al [55].	Systematic Review and Meta-analysis	NSPT in HD/PD patients	hs-CRP, IL-6, Alb, TNF-α, lipid markers	↓ hs-CRP (SMD = −1.53); IL-6 and Alb NS; TNF-α/lipids insufficient	NSPT moderately reduces inflammation in dialysis patients
15	Mizutani et al [56].	Prospective Cohort Study	Oral health status in HD patients	All-cause mortality	High DI-S → HR 3.04; more decayed teeth → HR 1.21; Periodontitis NS	Plaque and caries predict mortality in HD
16	Zhao et al [57].	Systematic Review and Meta-analysis (Interventional)	NSPT in CKD	eGFR, serum creatinine	Creatinine ↓ (fixed effect); eGFR unchanged	Evidence insufficient; more trials needed
17	Santos-Paul et al [52].	Prospective Study with Historical Controls	Periodontal treatment in kidney transplant waitlist patients vs. untreated historical controls	Cardiovascular events, coronary events, CV mortality, all-cause mortality	HR for CV events = 0.43; for coronary events = 0.31; for CV death = 0.43	Periodontal treatment reduced CV events and deaths
18	Kapellas et al [44].	Systematic Review and Meta-analysis	Bidirectional Periodontitis–CKD	ORs	OR = 1.60 (CKD in PD); OR = 1.69 (Periodontitis in CKD, NS)	Periodontitis is more likely to precede CKD
19	Deschamps-Lenhardt et al [21].	Systematic Review and Meta-analysis	Periodontitis association and treatment in CKD	ORs, IRRs	OR = 2.39 (severe PD); IRR = 1.73	Periodontitis is independently associated with CKD
20	Zhang et al [58].	Meta-analysis of Cohort Studies	Periodontitis in CKD	All-cause and CVD mortality	RR = 1.25 (all-cause); RR = 1.30 (CVD, NS)	Periodontitis increases all-cause death in CKD; the CVD link is weak
21	Sharma et al [58].	Pilot Randomized Controlled Trial	Immediate vs. delayed intensive periodontal therapy in CKD patients	Feasibility outcomes, cardio-kidney health, periodontal, and patient-reported outcomes	60 patients to be randomized; follow-up over 18 months	Designed to inform a definitive trial
22	Grubbs et al [59].	Pilot RCT	Immediate vs. delayed NSPT	kidney, inflammatory biomarkers	46 enrolled; diverse, underserved population	Feasibility confirmed; pilot data to inform full trial
23	Jamieson et al [60].	RCT	PT in Aboriginal CKD	cIMT, CKD progression, mortality	Ongoing; N = 600	First large RCT in underserved CKD
24	Fang et al [61].	6-Month Randomized Controlled Clinical Trial	NSPT in ESKD patients vs. no intervention	Periodontal parameters, hs-CRP, IL-6, ferritin, albumin, creatinine, BUN, transferrin	Significant ↓ in hs-CRP, IL-6; ↑ in nutritional markers; improved periodontal status	NSPT improves oral and systemic health in ESKD
25	Ruospo et al [62].	Systematic Review	Oral disease in CKD	Edentulism, Periodontitis, dry mouth	Periodontitis prevalence = 56.8% (CKD5D)	Oral disease is neglected in CKD patients
26	Chambrone et al [63].	Systematic Review and Meta-analysis	Periodontitis and PT in CKD	eGFR, Periodontitis–CKD association	OR = 1.65; eGFR ↑ with PT	PT is beneficial for CKD outcomes
27	Strippoli et al [64].	Prospective Multinational Cohort Study	Baseline oral exam in HD patients; follow-up on mortality/CVD	Prevalence of oral disease, mortality, hospitalizations, and CVD events	4500 patients across Europe and South America enrolled	Designed to assess associations between oral disease and mortality/CVD in HD
28	Wehmeyer et al [16].	Randomized Controlled Trial	Intensive periodontal therapy in ESKD patients	Periodontal parameters, IL-6, serum albumin	Periodontal improvements at 3 months; systemic markers NS	Feasible and safe; systemic effects inconclusive
29	Graziani et al [65].	Exploratory Trial	NSPT in GCP patients	GFR via cystatin C & MDRD; CRP, D-dimer, SAA, fibrinogen	↓ Cystatin C; MDRD unchanged; transient ↑ CRP/SAA	NSPT may improve GFR via cystatin C
30	Bayraktar et al [66].	Cross-sectional Observational Study	Comparison of Periodontitis in HD and controls	SFR, SpH, SBC, DMFT, PI, CRP	Higher DMFT in Periodontitis; lowest SFR in HD; PI and CRP elevated	Oral disease may drive inflammation in ESKD

Abbreviations: CKD, Chronic Kidney Disease; ESKD, End-Stage Kidney Disease; HD, Hemodialysis; PT, Periodontal Therapy; NSPT, Non-Surgical Periodontal Therapy; GCP, Generalized Chronic Periodontitis; GFR, Glomerular Filtration Rate; MDRD, Modification of Diet in Renal Disease (equation); CRP, C-Reactive Protein; hs-CRP, High-Sensitivity C-Reactive Protein; IL-6, Interleukin-6; SAA, Serum Amyloid A; DMFT, Decayed, Missing, and Filled Teeth Index; PI, Plaque Index; SBC, Salivary Buffering Capacity; SpH, Salivary pH; SFR, Salivary Flow Rate; CAL, Clinical Attachment Level; PPD, Periodontal Probing Depth; GI, Gingival Index; DI-S, Debris Index – Simplified; HR, Hazard Ratio; OR, Odds Ratio; RR, Relative Risk; IRR, Incidence Rate Ratio; SMD, Standardized Mean Difference; NS, Not Significant

A. Bidirectional relationships between periodontal disease and CKD

Periodontal inflammation and chronic kidney disease (CKD) are linked through a dynamic, bidirectional network of immune, vascular, metabolic, and microbial pathways that mutually reinforce disease progression [21, 44]. In turn, CKD-associated metabolic acidosis, uremia, and impaired neutrophil function diminish oral host defenses, worsening periodontal pathology [42]. In periodontitis, disruption of epithelial barrier integrity within periodontal pockets allows sustained translocation of oral pathogens, lipopolysaccharide (LPS), and host-derived inflammatory mediators into the systemic circulation [67]. This chronic inflammatory spillover activates complement pathways, primes circulating neutrophils, and induces endothelial dysfunction, collectively promoting oxidative stress and microvascular injury. Within the kidney, these systemic insults preferentially target the glomerular endothelium and peritubular capillary network, amplifying leukocyte recruitment, complement deposition, and cytokine-driven tubulointerstitial inflammation [36].

Immune dysregulation represents a central axis of reciprocity. Periodontitis induces maladaptive innate and adaptive immune responses characterized by persistent neutrophil activation, exaggerated NET formation, and TH17 skewing, with sustained production of IL-17, TNF-α, and IL-6 [68]. These immune perturbations extend beyond the oral niche, shaping a systemic inflammatory phenotype that lowers renal injury thresholds and impairs resolution of kidney inflammation. Conversely, CKD is itself a state of immune dysfunction marked by uremia-induced neutrophil paralysis, T-cell exhaustion, and chronic low-grade immune activation [69]. This paradoxical immune state diminishes effective antimicrobial surveillance in the oral cavity while heightening inflammatory reactivity to periodontal antigens, thereby accelerating periodontal tissue destruction and perpetuating microbial dysbiosis.

Vascular and bone remodeling pathways further couple periodontal disease and CKD. Periodontitis-driven RANKL overexpression promotes alveolar bone resorption, while CKD-associated mineral bone disorder amplifies systemic RANKL–Osteoprotegerin imbalance, vascular calcification, and skeletal fragility [70]. Shared signaling pathways link alveolar bone loss to renal osteodystrophy and arterial stiffening, with endothelial dysfunction acting as a common upstream mediator. These vascular changes impair gingival and renal microcirculation alike, exacerbating hypoxia, inflammation, and tissue remodeling in both organs.

Microbiome and metabolic disturbances provide an additional reinforcing layer. Periodontal dysbiosis enriches keystone pathogens capable of immune subversion, while CKD-associated uremic dysbiosis alters the gut–oral axis through accumulation of uremic toxins, impaired epithelial barriers, and altered microbial metabolism [71]. Systemic dissemination of microbial products, including LPS and other pathogen-associated molecular patterns, sustains chronic inflammation and metabolic stress, further injuring renal and periodontal tissues. Importantly, reduced renal clearance of inflammatory mediators and microbial metabolites in CKD magnifies their systemic persistence, intensifying periodontal inflammation and closing a self-amplifying pathogenic loop.

Collectively, these mechanisms establish that periodontal disease and CKD are biologically interconnected rather than parallel comorbidities. Periodontal inflammation acts as a chronic inflammatory and microbial stressor that accelerates renal injury, while CKD fosters immune, vascular, and metabolic environments that exacerbate periodontal breakdown. This reciprocal, self-sustaining interaction underscores the need for integrated oral–renal risk assessment and positions periodontal inflammation as a potentially modifiable contributor to CKD progression.

B. Therapeutic modifiability

Interventional trials show that NSPT reduces systemic inflammatory markers, including CRP, IL-6, and ferritin, and modestly improves eGFR and nutritional indicators in CKD cohorts [63, 65, 72]. While long-term renal outcomes remain uncertain, these results indicate partial reversibility of the inflammatory burden characteristic of CKD. Mechanistically, periodontal therapy may downregulate endothelial activation and enhance cystatin C-based filtration measures, offering insight into systemic benefits beyond the oral cavity. Sustained longitudinal studies are still needed to confirm causal pathways and quantify the magnitude of the benefit.

Conversely, there is some evidence that treating CKD may modify the periodontal inflammation and disease trajectory through improvements in immune competence, metabolic homeostasis, and vascular health; however, there is a paucity of data to support this association [73]. Mechanistically, optimization of uremic toxin clearance with intensified or adequate dialysis can reduce systemic cytokine levels, oxidative stress, and neutrophil dysfunction, changes that may partially restore effective antimicrobial defense within the periodontal niche and attenuate gingival inflammation [74]. Similarly, correction of CKD-related anemia and metabolic acidosis improves tissue oxygenation and local pH, potentially limiting hypoxia-driven inflammatory signaling and protease activity in periodontal tissues. Management of chronic kidney disease–mineral bone disorder (CKD-MBD) may further influence periodontal outcomes, as normalization of calcium–phosphate balance, suppression of secondary hyperparathyroidism, and vitamin D supplementation can mitigate RANKL-mediated alveolar bone resorption [75–78]. Observational data from dialysis cohorts and kidney transplant recipients suggest that improvement in renal function or uremic control is associated with stabilization or modest improvement in periodontal indices, although immunosuppressive therapy introduces heterogeneity in post-transplant populations. It’s important to acknowledge that periodontal disease is influenced not only by CKD itself but also by its underlying causes, such as diabetes and glomerulonephritis, which independently exacerbate immune and microvascular dysfunction; collectively, these observations support a reciprocal therapeutic framework in which addressing both CKD and its etiologic drivers may dampen periodontal inflammation and slow disease progression, reinforcing bidirectional modifiability across the oral–renal axis and the need for integrated interventional studies.

C. Advanced disease states: dialysis and transplant populations (Table 2 and Table 3)

Table 2.

Oral manifestations in patients with a kidney transplant

Category	Oral manifestations/findings	Underlying mechanisms or contributing factors	Clinical implications/management considerations
Soft-tissue lesions [79, 80].	Gingival overgrowth, mucosal hyperplasia	Cyclosporine, calcium-channel blockers, and tacrolimus–induced fibroblast activation and altered collagen metabolism	Maintain meticulous plaque control; consider drug substitution or gingivectomy for severe cases
Infectious lesions [80, 81].	Candidiasis, herpes simplex, cytomegalovirus ulcerations	Long-term immunosuppression, xerostomia, altered oral flora	Topical/systemic antifungal or antiviral therapy; adjust immunosuppressive dosage in consultation with transplant team
Mucosal and salivary changes [79, 82].	Xerostomia, burning mouth, taste disturbance	Reduced salivary flow from anticholinergic or calcineurin-inhibitor effects	Saliva substitutes, topical fluoride, antifungal prophylaxis as indicated
Neoplastic/premalignant lesions [80].	Oral squamous-cell carcinoma, leukoplakia, hairy leukoplakia	Oncogenic viral reactivation (EBV, HPV) under chronic immunosuppression	Regular oral-cancer screening; biopsy suspicious lesions; patient self-inspection education
Periodontal disease [79, 83].	Increased plaque index, attachment loss, delayed wound healing	Impaired immune response, microangiopathy, altered neutrophil function	Periodontal maintenance every 3–6 months; avoid surgical procedures during high-dose immunosuppression

Table 3.

Oral manifestations in patients on dialysis [84–86].

Category	Oral/dental manifestation	Typical features	Likely etiology or association
Infectious – Fungal	Oral candidiasis (pseudomembranous, erythematous, angular cheilitis)	White plaques that wipe off; erythematous or burning mucosa; angular fissures	Xerostomia, immunosuppression, poor hygiene, antibiotic use
	Deep fungal infections (rare)	Necrotic ulcers, black eschar, facial pain	Severe immunosuppression (ESRD with diabetes, malnutrition)
Infectious (Viral)	Herpes simplex/zoster reactivation	Painful vesicles or ulcers; unilateral zoster lesions	Uremia-related immune dysfunction
	Hepatitis B/C–associated mucosal lesions	Lichenoid changes, petechiae, bleeding tendency	Chronic viral hepatitis (common in long-term dialysis)
Infectious (Bacterial)	Periodontitis/necrotizing ulcerative gingivitis	Bleeding, pain, necrosis, attachment loss	Uremic immune dysfunction, altered salivary composition
	Secondary oral infections (uremic milieu)	Diffuse erythema, halitosis, delayed healing	Elevated urea/ammonia levels; altered microbiome
Metabolic/Uremic	Uremic stomatitis	Painful erythematous or ulcerative lesions with pseudo membranes; ammonia odor	Severe azotemia (BUN > 150 mg/dL); poor dialysis adequacy
	Ammonia-like halitosis	Fetid uremic odor	Breakdown of urea to ammonia in saliva
Hematologic/Vascular	Gingival bleeding, petechiae, ecchymoses	Spontaneous or post-procedural bleeding	Uremic platelet dysfunction; heparin exposure during dialysis
	Pallor of oral mucosa	Pale mucosa, tongue, lips	Anemia of CKD
	Uremic calcifications/metastatic calcinosis	Hard nodules, limited jaw motion (rare)	Secondary hyperparathyroidism; calcium–phosphate imbalance
Salivary/Glandular	Xerostomia (salivary hypofunction)	Dry mucosa, dysgeusia, caries, burning	Fluid restriction, polypharmacy, uremia
	Sialadenitis/parotid enlargement	Painful or painless gland swelling	Dehydration, secondary hyperparathyroidism
Drug-related	Xerostomia/dysgeusia	Metallic taste, dry mouth	Antihypertensives, phosphate binders, diuretics
	Lichenoid drug reactions	Reticular or erosive lesions	ACE inhibitors, β-blockers, allopurinol
	Mucositis/ulcerations	Diffuse painful erosions	Immunosuppressants or inadequate renal drug clearance
Bone/Mineral (Renal Osteodystrophy)	Loss of lamina dura/“ground-glass” appearance	Generalized bone demineralization; jaw enlargement	Secondary hyperparathyroidism; altered Ca–P metabolism
	Metastatic calcifications (soft tissues)	Firm white deposits; mucosal irritation	Hypercalcemia, phosphate retention
	Medication-related osteonecrosis (MRONJ)	Exposed bone > 8 weeks; pain; delayed healing	Bisphosphonate/denosumab exposure in CKD-MBD
Dental/Hard Tissue	Caries (root/cervical)	Rapid progression, especially with xerostomia	Salivary dysfunction; high urea content
	Tooth wear/erosion	Smooth cupped lesions; sensitivity	Dietary acids, GERD, xerostomia
	Enamel hypoplasia/delayed eruption (pediatric CKD)	Thin, discolored enamel; delayed eruption	Disturbed Ca–P balance; growth delay
Neuropathic/Sensory	Dysgeusia/metallic taste/burning mouth	Taste alteration; burning with normal mucosa	Uremia, xerostomia, zinc deficiency
	Peripheral neuropathic oral pain	Burning or tingling sensations	Uremic neuropathy

Patients undergoing kidney replacement therapy (KRT), hemodialysis, peritoneal dialysis, or post-transplant bear a disproportionate oral-disease burden due to immunosuppression, polypharmacy, and limited dental access [51, 52]. Periodontal treatment among transplant candidates has been associated with lower cardiovascular event rates and mortality [23]. Despite this evidence, standardized dental integration within dialysis and transplant protocols remains rare, highlighting a major implementation gap.

D. Converging risk pathways

CKD and periodontitis share common upstream determinants, including socioeconomic disadvantage, diabetes mellitus (DM), malnutrition, and tobacco exposure. Emerging data reveal overlapping dysbiosis of the oral-gut microbiome and immune-metabolic disruptions [87–90]. Microbial translocation and impaired epithelial barriers amplify systemic inflammation, reinforcing the bidirectional loop between oral and renal dysfunction [90].

Collectively, current evidence delineates a dynamic inflammatory feedback system linking the oral cavity and kidneys. Periodontitis intensifies systemic inflammation and endothelial injury, while CKD impairs oral healing and immunity. Non-surgical periodontal therapy demonstrates partial biological reversibility, warranting its inclusion in multidisciplinary renal-care models. Recognizing oral health as an intrinsic component of kidney care is thus both biologically justified and clinically imperative.

Oral health across the lifespan of kidney disease (Table 4)

Table 4.

Oral manifestations and pathophysiologic correlates across chronic kidney disease (CKD) stages

CKD Stage	eGFR (mL/min/1.73 m2)	Key Oral Findings	CKD-MBD and Systemic Correlates	Relative Periodontal Risk
Stage 1	>90 (normal)	Mild xerostomia	Minimal bone impact	Low
Stage 2	60–89	Xerostomia, metallic taste	Initial PTH fluctuations	Modest
Stage 3a	45–59	Uremic fetor, dysgeusia	Early alveolar bone thinning	Moderate
Stage 3b	30–44	Mucosal pallor, tooth mobility	Bone demineralization	High
Stage 4	15–29	Stomatitis, ammonia odor	Osteodystrophy and radiographic “ground-glass” changes	High
Stage 5 (ND)	<15 (non-dialysis)	Ulcerations, gingival bleeding	Prominent osteodystrophy and secondary hyperparathyroidism	Severe
Stage 5D (Dialysis)	<15 + dialysis	Gingival overgrowth, petechiae, jaw fragility	Advanced bone loss and high fracture risk	Advanced

Oral health outcomes evolve dynamically along the CKD continuum, with pathological changes becoming more pronounced as renal function declines. These manifestations are both clinical reflections and pathophysiologic consequences of systemic metabolic, immunologic, and mineral disturbances. They provide a visible window into the inflammatory and bone-mineral alterations underlying CKD progression.

Stage-specific patterns and care integration

In advanced CKD (stages 4–5 ND), patients often present with stomatitis, mucosal ulcerations, and bleeding diathesis secondary to uremic platelet dysfunction and anemia [49]. The severity of periodontal and mucosal lesions parallels metabolic disturbances in calcium, phosphate, and PTH. Once dialysis is initiated (CKD 5D), oral complications such as gingival overgrowth, petechiae, and jawbone fragility become prominent, necessitating the coordinated scheduling of dental procedures around dialysis sessions and adjustments to anticoagulation exposure. These observations underscore that oral health trajectories in CKD are not isolated clinical curiosities but systemic markers of disease progression. The integration of dental assessment within nephrology care, particularly at the initiation of dialysis or during transplant evaluation, presents an actionable opportunity for prevention and early intervention.

Bone and mineral interactions in oral disease (Fig. 3)

Fig. 3.

Bone and mineral interactions in oral disease

CKD-MBD arises from dysregulated calcium-phosphate and parathyroid hormone–fibroblast growth factor-23 (PTH-FGF-23) signaling [91]. FGF-23 elevations appear early, promoting phosphate excretion but driving secondary hyperparathyroidism and vascular calcification. When eGFR falls below 45–50 mL/min, hyperphosphatemia, hypocalcemia, and elevated PTH lead to skeletal remodeling disorders, including osteitis fibrosa, osteomalacia, and mixed uremic osteodystrophy [92, 93]. Oral manifestations include jawbone demineralization, “ground-glass” radiographic appearance, and, in severe high-turnover states, brown-tumor-like lesions [94]. These findings underscore the diagnostic potential of oral radiography in revealing systemic bone pathology and guiding multidisciplinary management.

Soft-tissue and pharmacologic complications

Up to 90% of patients with CKD exhibit oral soft-tissue alterations [95]. Xerostomia, one of the most prevalent conditions, results from salivary hypofunction and fluid restriction [82, 96]. and predisposes individuals to mucosal discomfort, dysgeusia, and caries [97, 98]. Opportunistic infections such as candidiasis arise from immune compromise and prolonged antibiotic exposure [99]. Pharmacologic regimens, including cyclosporine, calcium-channel blockers, and renin-angiotensin inhibitors, commonly induce drug-induced gingival overgrowth (DIGO), with a prevalence ranging from 6% to 80%, depending on the drug class [79, 80, 100–104].The condition impairs mastication, plaque control, and speech, thereby reinforcing an inflammatory feedback loop. Clinical management emphasizes stringent plaque control, medication review, and surgical correction for severe cases; periodontal therapy should be scheduled during periods of stable hemodynamics and minimal immunosuppressive load.

Dental indices and oral health status in chronic kidney disease

Dental indices provide objective, quantifiable measures of oral disease burden and inflammation, offering insights into systemic health in individuals with chronic kidney disease (CKD). Standard indices, including the Decayed, Missing, and Filled Teeth (DMFT) index, Plaque Index (PI), Gingival Index (GI), and Clinical Attachment Level (CAL), have been widely used to assess oral health in CKD populations [16, 64].

1. Quantitative evidence of oral disease burden

Cross-sectional and cohort studies consistently demonstrate higher DMFT and PI scores in CKD and end-stage kidney disease (ESKD) cohorts compared with healthy controls, indicating increased caries prevalence and suboptimal plaque control [62, 105, 106]. Gingival inflammation, reflected in elevated GI and bleeding on probing, correlates with declining renal function and elevated systemic inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) [50]. Meta-analyses reveal that periodontitis severity, as measured by CAL and probing pocket depth (PPD), worsens in parallel with reduced eGFR [47, 54]. In advanced CKD, periodontal destruction appears accelerated, potentially mediated by immune dysregulation, uremic toxins, and secondary hyperparathyroidism.

2. Salivary and microbiological parameters

Beyond classical dental indices, salivary parameters serve as complementary markers of both systemic and oral health. CKD patients frequently exhibit reduced salivary flow rate (SFR) and altered pH (SpH), predisposing to xerostomia, mucosal lesions, and dysbiosis [66, 95]. Salivary CRP and urea concentrations increase with CKD stage, correlating with systemic inflammatory burden [97]. Microbiological profiling reveals an enrichment of Porphyromonas gingivalis, Tannerella forsythia, and Prevotella intermedia in CKD and dialysis cohorts, linking uremic environments to the proliferation of periodontal pathogens [88, 89]. These microbial shifts correspond with higher plaque indices and systemic inflammation, reinforcing the oral–systemic inflammatory axis.

3. Periodontal therapy and oral indices

Interventional evidence supports partial reversibility of oral and systemic inflammation through non-surgical periodontal therapy (NSPT). Post-NSPT improvements in GI, PI, and PPD are consistently accompanied by reductions in CRP, IL-6, and malondialdehyde (MDA) [50, 53, 63, 65, 72]. In ESKD populations, NSPT yields transient reductions in inflammatory biomarkers and modest improvements in nutritional indicators (albumin, hemoglobin), but long-term effects on renal outcomes remain uncertain [51, 52, 55, 57, 61]. Nonetheless, these findings substantiate the role of oral therapy as a feasible adjunct to CKD care.

4. Clinical implications and research gaps

Elevated dental indices in CKD signal more than localized pathology; they represent measurable markers of systemic inflammation, endothelial dysfunction, and cardiovascular risk. Standardizing oral health metrics in nephrology clinics could facilitate the earlier detection of inflammatory burden and improve interprofessional coordination. However, heterogeneity in study design, small sample sizes, and inconsistent calibration of dental indices limit comparability across studies [59, 107]. Future research should prioritize standardized periodontal assessments and longitudinal integration of oral indices into CKD management and registries.

Clinical implications

Periodontitis independently contributes to systemic inflammation and mortality among patients with CKD. Meta-analytic data link periodontal disease to elevated CRP, hypoalbuminemia, cardiovascular disease, and all-cause mortality, with pooled risk estimates ranging from 1.2 to 2.5 [46, 61]. Maintaining oral hygiene, including twice-daily toothbrushing, is associated with reduced incidence of diabetes, slower eGFR decline, and lower cardiovascular risk [47, 48, 108]. These findings situate oral hygiene as a modifiable behavioral determinant of systemic inflammation, vascular function, and metabolic control.

Recognizing stage-specific oral patterns enhances the early detection of CKD and improves multidisciplinary care planning. Routine inclusion of oral health assessment in nephrology visits can identify CKD-related inflammation before biochemical markers shift. As evidence linking oral findings to systemic outcomes continues to strengthen, these manifestations may function as low-cost, non-invasive indicators of systemic disease activity.

Global and structural inequities in oral–renal health

Chronic kidney disease (CKD) and oral diseases disproportionately affect low- and middle-income countries (LMICs), where resource scarcity, fragmented health systems, and limited preventive infrastructure converge to accelerate morbidity. Nearly 80% of individuals with CKD live in LMICs, yet access to nephrology services and oral healthcare remains severely constrained [8–10].

1. Health system fragmentation and access barriers

In many LMICs, dental and renal care operate in parallel but disconnected systems. Oral health services are often excluded from universal health coverage (UHC) packages, leading to out-of-pocket costs that deter care-seeking [46, 109, 110]. Geographic maldistribution of dental professionals further compounds inequity in rural and peri-urban regions, frequently having fewer than one dentist per 50,000 people, while dialysis centers cluster in tertiary urban hospitals [111, 112]. This service separation reinforces the invisibility of oral disease in CKD management and prevents early identification of systemic inflammation.

2. Sociodemographic and cultural determinants

Structural inequities intersect with gender, education, and socioeconomic status. Women and lower-income groups experience higher rates of untreated dental decay and delayed CKD diagnosis, reflecting the combined influence of gendered caregiving roles and constrained financial autonomy [73, 109]. Cultural perceptions of oral health as a cosmetic rather than medical concern also impede integration into chronic disease care models, a misconception exacerbated by limited community-level health literacy [81].

3. Workforce and training deficits

The shortage of oral-health professionals trained in systemic-disease management represents a key bottleneck to interdisciplinary care. Few nephrology curricula incorporate oral–systemic education, and most dental programs lack training on managing medically complex patients [24, 25]. Expanding interprofessional education linking dental, public health, and nephrology disciplines could reduce care gaps and strengthen surveillance of oral indicators of systemic disease.

4. Data and policy gaps

Current global surveillance frameworks for CKD and oral health remain siloed. The World Health Organization’s 2023–2030 NCD Implementation Roadmap recognizes oral diseases but lacks indicators that link oral inflammation with renal or cardiovascular outcomes [113]. Integrating oral-health variables (e.g., DMFT, CRP-linked indices) into CKD registries could improve disease monitoring and policy targeting. Furthermore, existing policy investments favor dialysis expansion over preventive approaches. Redirecting resources toward community-based oral–renal screening programs and integrating oral health into essential NCD packages could yield more equitable health outcomes.

5. Global solidarity and research imperatives

Equity-oriented collaboration is critical to dismantling structural asymmetries between research institutions in the Global North and South. Capacity-building efforts such as bilateral training, shared data infrastructure, and equitable authorship practices can counter the prevailing concentration of oral–renal research in high-income contexts [88, 90]. Future global consortia should prioritize participatory research approaches that amplify community and patient voices, aligning with the WHO’s call for people-centered oral health within the NCD framework.

Integrated models and implementation pathways for oral–renal health (Table 5)

Table 5.

Author-synthesized Recommendations for oral–renal care integration across the CKD continuum [21, 23, 48, 63, 65, 79, 81, 91, 93, 94, 100, 103, 108–110, 112, 114, 115].

CKD Stage/Context	Author-Synthesized Recommendations
Early CKD (Stages 1–2)	• Incorporate dental screening into annual CKD visits. • Reinforce twice-daily brushing and moderate dietary phosphate. • Record baseline oral indices (DMFT, PI, GI) for longitudinal tracking.
Moderate CKD (Stages 3a–3b)	• Screen for xerostomia/dysgeusia; use saliva substitutes and fluoride rinses. • Monitor CKD-MBD markers and coordinate dental hygiene with nephrology care. • Apply NSPT to reduce CRP and IL-6.
Advanced CKD (Stage 4)	• Perform dental procedures on non-dialysis days; avoid nephrotoxic anesthetics. • Implement antimicrobial rinses and topical fluoride. • Engage interdisciplinary review for bone changes.
End-Stage CKD (Stage 5 ND/5D)	• Schedule invasive care ≥ 24 h post-dialysis; coordinate anticoagulation. • Manage DIGO via plaque control and medication review. • Use local hemostatic measures and antibiotics only when indicated.
Transplant Candidates/Recipients	• Require full dental clearance pre-transplant. • Treat chronic oral infection foci before surgery. • Post-transplant: monitor for fungal/viral lesions and DIGO in collaboration with transplant teams.
Global/Policy Level	• Embed oral health into CKD guidelines and UHC packages. • Expand interprofessional training linking nephrology and dentistry.

Note. Recommendations synthesized from evidence summarized in Tables 1–3 and cited PMIDs. They represent the authors’ interpretation of the literature rather than established clinical guidelines. Abbreviations: CKD = chronic kidney disease; MBD = mineral and bone disorder; DMFT = Decayed, Missing, Filled Teeth Index; PI = Plaque Index; GI = Gingival Index; NSPT = non-surgical periodontal therapy; CRP = C-reactive protein; DIGO = drug-induced gingival overgrowth; EHR = electronic health record; UHC = universal health coverage; LMICs = low- and middle-income countries

Efforts to integrate oral health within kidney care are emerging but remain fragmented across regions. Existing initiatives demonstrate that when oral–renal coordination is systematized, measurable benefits occur in inflammation control, cardiovascular outcomes, and patient-reported quality of life [24, 26].

1. Established models of integration

Several countries have piloted or institutionalized frameworks that connect nephrology and dental services.

1. Japan maintains one of the most mature hospital-based systems, embedding routine oral evaluations within dialysis units and reporting reductions in infection-related hospitalizations [56].

2. Brazil’s public health system, through the Estratégia Saúde da Família, integrates oral and chronic disease management at the community level, enhancing preventive outreach in high-risk populations [116].

3. The United Kingdom has adopted shared care pathways between National Health Service (NHS) dental and renal clinics, with cross-referral protocols that emphasize infection control before transplantation [117].

4. The United States remains largely fee-for-service, though isolated pilot programs such as tele dentistry supported dialysis centers demonstrate feasibility for scaling integrated prevention models [118].

2. Digital and informatics integration

Electronic health records (EHRs) and interoperable informatics systems provide a critical mechanism for embedding oral assessments into CKD workflows. Linking oral indices (DMFT, GI, PI) and biomarker data (CRP, IL-6) to nephrology EHRs enables earlier identification of systemic inflammation and facilitates interprofessional communication [45, 112, 119]. Decision-support tools can generate prompts for dental referral when risk thresholds are exceeded, while teleconsultation platforms extend access to rural or dialysis-based populations [111, 120].

3. Workforce and training integration

Interprofessional education remains foundational to sustainable integration. Curricula combining nephrology, dental hygiene, and public health competencies have demonstrated improvements in student self-efficacy and collaborative readiness [24, 25, 121]. In high-income settings, integrated residency or fellowship programs linking oral medicine and nephrology can improve patient continuity and safety.

4. Implementation science and sustainability

Translating evidence into durable systems requires context-specific adaptation guided by implementation science principles: feasibility, acceptability, fidelity, and equity. Pilot projects in Japan, Brazil, and the United States illustrate diverse models, yet few have undergone scale-up evaluation. Cost-effectiveness analyses suggest integration is economically viable when paired with reductions in hospitalization and infection-related events [122]. In LMICs, sustainability will depend on leveraging community health workers, mobile dentistry, and simplified referral algorithms to address workforce scarcity and infrastructure limitations.

Drawing on the clinical evidence, inequities, and implementation challenges summarized above, the following table outlines the author’s synthesized recommendations for embedding oral–renal integration within clinical, educational, and policy frameworks.

Innovations in integrated oral-nephrology care

Advances in digital health, precision medicine, and community-based interventions have significantly improved the integration of oral care within nephrology settings. Health informatics tools, such as electronic health records (EHRs) and machine learning algorithms, now facilitate the identification of oral frailty as an early indicator of renal decline, enabling timely multidisciplinary interventions [123, 124].

Recent microbiome research highlights distinct oral microbial profiles in CKD patients, suggesting novel diagnostic and monitoring pathways through salivary biomarkers and predictive analytics [125, 126]. Concurrently, genomic and bioinformatics approaches have identified shared inflammatory pathways linking periodontitis with renal and cardiovascular conditions, supporting personalized risk assessments and targeted therapeutic strategies [127, 128].

Community and telehealth models demonstrate reduced systemic inflammation and enhanced patient outcomes through proactive, coordinated oral–renal care. Such informatics-driven, interdisciplinary innovations underscore the feasibility and clinical value of integrating oral health into routine nephrology care, particularly within vulnerable and underserved populations [60].

Research and policy opportunities

Despite growing evidence associating oral disease with CKD progression and transplant outcomes, standardized dental management protocols remain lacking, especially for kidney transplant candidates [129]. Surveys across transplant centers reveal substantial variability in pre-transplant dental screening practices, dental infection strategies, and the use of prophylactic antibiotics [129]. These variations highlight the critical need for well-defined clinical guidelines and standardized criteria to ensure patient safety and quality of care. Additional multicenter, longitudinal studies are urgently needed to inform optimal timing, scope, and clinical outcomes of dental interventions before and after transplantation.

Parallel mechanistic research is necessary to elucidate the biological pathways linking periodontal inflammation, microbial dysbiosis, and systemic immune activation with kidney outcomes, such as graft rejection, proteinuria, and cardiovascular complications [22]. Such research will form the scientific basis for clinical guidelines and personalized risk assessment tools tailored to CKD populations.

Implementation science represents another promising avenue for scaling oral–renal care integration. Studying real-world barriers and facilitators, including referral processes, reimbursement policies, and provider capacity, will facilitate adaptation and broader implementation of integrated care models across diverse healthcare systems [130]. Concurrently, improving electronic medical record (EMR) interoperability could streamline monitoring of oral-systemic risk factors, automate dental referrals, and enhance shared care planning between nephrology and dental professionals [131, 132].

Policy development and workforce capacity building are crucial for integrating oral health into broader NCD strategies. Revising Universal Health Coverage (UHC) benefit packages to include dental care for high-risk CKD populations and integrating oral–systemic education into interprofessional training programs are actionable policy initiatives [111]. Crucially, equity must be the anchor of these efforts. Populations disproportionately affected by socioeconomic, geographic, or systemic barriers to dental and kidney care must be prioritized within research, policy, and implementation frameworks [133]. Together, these research and policy opportunities provide a clear roadmap towards preventive, evidence-based kidney care, recognizing oral health as an essential determinant of both systemic and transplantation-related outcomes. The authors provide a framework of oral–renal care integration across the CKD continuum in Table 6.

Table 6.

Author’s clinical Recommendations for dental and oral health management in patients on dialysis and after kidney transplant [79, 80, 83–86, 109].

Clinical Context	Author’s Recommendations
Dialysis: Appointment timing and planning	Schedule procedures on non-dialysis days; allow ≥ 24 h post-dialysis before invasive care; avoid sessions immediately after heparin use.
Dialysis: Bleeding and hematologic considerations	Obtain platelet count before surgery; avoid NSAIDs and aspirin; apply local hemostatic agents for bleeding control [85].
Dialysis: Xerostomia and caries prevention	Encourage hydration within limits; prescribe saliva substitutes; use high-fluoride toothpaste or varnish; recall every 3 months.
Dialysis: Infection control	Employ antiseptic mouthrinses (chlorhexidine 0.12%); ensure pre-procedural rinsing; consider antifungal prophylaxis for immunocompromised patients.
Dialysis: Bone and mineral disorders (CKD–MBD)	Defer elective extractions during active secondary hyperparathyroidism; use atraumatic surgical technique; monitor bone healing.
Dialysis: Pharmacologic safety	Adjust local anesthetic and analgesic doses for renal clearance; avoid nephrotoxic or renally excreted drugs (e.g., NSAIDs, aminoglycosides).
Transplant: Preoperative clearance	Perform comprehensive dental exam within 6 months prior to transplant; eliminate oral infection sources; issue dental clearance report.
Transplant: Early post-transplant (first 3–6 months)	Avoid elective dental care; manage mucositis symptomatically; use topical corticosteroids and anesthetics for comfort; liaise with transplant physician before invasive procedures.
Transplant: Long-term care	Manage drug-induced gingival enlargement via plaque control and professional scaling; consider drug substitution in collaboration with nephrology.
Transplant: Mucosal surveillance	Conduct biannual oral soft-tissue exams; biopsy suspicious lesions; emphasize patient self-examination education.
Transplant: Drug safety and infection prophylaxis	Delay elective care during high-dose immunosuppression; use antibiotic prophylaxis as per institutional protocols; monitor for delayed wound healing.
Shared across dialysis and transplant populations	Maintain consistent communication among nephrology, dental, and transplant teams through shared medical records and EHR prompts.

Note. Recommendations reflect authors’ synthesis of best practices drawn from Tables 3a–3b and the literature (PMIDs cited). They represent clinical guidance intended to complement professional judgment and local institutional policies. Abbreviations: CKD–MBD = chronic kidney disease–mineral and bone disorder; NSAIDs = nonsteroidal anti-inflammatory drugs; EHR = electronic health record

Conclusion

Periodontal disease and chronic kidney disease appear to be interlinked systemic conditions, driven by shared inflammatory pathways and microbial dysbiosis, although current evidence is largely observational with modest effect sizes and mechanisms shared with other chronic inflammatory diseases.

Recognizing periodontitis as a potentially modifiable risk marker for kidney outcomes supports integrating standardized oral assessments into CKD risk stratification and earlier detection, alongside broader integration of oral healthcare within nephrology practice through interdisciplinary collaboration and health-system innovations. Prospective cohort studies and adequately powered interventional trials are needed to clarify causality and quantify the kidney-specific benefits of periodontal therapy. Future research should prioritize implementation science to translate current evidence into practical interventions, ultimately improving patient outcomes and advancing equitable, holistic care.

Author contributions

PG: conceptualization, original draft, literature search & screening, writing original draft, project administration, EC: draft, review & editing, AD: draft, review & editing SM: draft, review & editing, RV: draft, review & editing, IL: draft, review and editing, EL: draft, review and editing, LS: draft, review and supervision PG: conceptualization, literature search & screening, writing original draft, review, editing & supervision.

Funding

None.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics and consent to participate declarations

not applicable.

Disclosure

PG, EC, IL, AD, SM, RV, LS: nothing to disclose, EL: Speaker Bureau: Novo Nordisk, Opko, Otsuka, Vertex, Advisory Board: Astra Zeneca, Natera, Otsuka, Travere, Vera, Vertex, PG: Serves as Deputy Editor for the American Society of Nephrology’s Kidney News and as an Editorial Board Member for Advances in Kidney Disease and Health and BMC Nephrology. Member of the Medical Advisory Board for the National Kidney Foundation–Ohio and the Advisory Boards of Akebia Therapeutics and Amgen.

Competing interests

The authors declare no competing interests.