This review highlights oral anomalies with major clinical impact in Addison disease (AD), including dental health and dermatologic features, through a dual perspective: pigmentation issues and AD comorbidities with oral manifestations. Affecting 92% of AD patients, cutaneomucosal hyperpigmentation is synchronous with or precedes general manifestations by up to a decade, underlying melanocytic infiltration of the basal epidermal layer; melanophages in the superficial dermis; and, rarely, acanthosis, perivascular lymphocytic infiltrate, and hyperkeratosis. Intraoral pigmentation might be the only sign of AD; thus, early recognition is mandatory, and biopsy is helpful in selected cases. The buccal area is the most affected location; other sites are palatine arches, lips, gums, and tongue. Pigmented oral lesions are patchy or diffuse; mostly asymptomatic; and occasionally accompanied by pain, itchiness, and burn-like lesions. Pigmented lingual patches are isolated or multiple, located on dorsal and lateral areas; fungiform pigmented papillae are also reported in AD individuals. Dermoscopy examination is particularly indicated for fungal etiology; yet, it is not routinely performed. AD’s comorbidity burden includes the cluster of autoimmune polyglandular syndrome (APS) type 1 underlying AIRE gene malfunction. Chronic cutaneomucosal candidiasis (CMC), including oral CMC, represents the first sign of APS1 in 70–80% of cases, displaying autoantibodies against interleukin (IL)-17A, IL-17F ± IL-22, and probably a high mucosal concentration of interferon (IFN)-γ. CMC is prone to systemic candidiasis, representing a procarcinogenic status due to Th17 cell anomalies. In APS1, the first cause of mortality is infections (24%), followed by oral and esophageal cancers (15%). Autoimmune hypoparathyroidism (HyP) is the earliest endocrine element in APS1; a combination of CMC by the age of 5 years and dental enamel hypoplasia (the most frequent dental complication of pediatric HyP) by the age of 15 is an indication for HyP assessment. Children with HyP might experience short dental roots, enamel opacities, hypodontia, and eruption dysfunctions. Copresence of APS-related type 1 diabetes mellitus (DM) enhances the risk of CMC, as well as periodontal disease (PD). Anemia-related mucosal pallor is related to DM, hypothyroidism, hypogonadism, corresponding gastroenterological diseases (Crohn’s disease also presents oral ulceration (OU), mucogingivitis, and a 2–3 times higher risk of PD; Biermer anemia might cause hyperpigmentation by itself), and rheumatologic diseases (lupus induces OU, honeycomb plaques, keratotic plaques, angular cheilitis, buccal petechial lesions, and PD). In more than half of the patients, associated vitiligo involves depigmentation of oral mucosa at different levels (palatal, gingival, alveolar, buccal mucosa, and lips). Celiac disease may manifest xerostomia, dry lips, OU, sialadenitis, recurrent aphthous stomatitis and dental enamel defects in children, a higher prevalence of caries and dentin sensitivity, and gingival bleeding. Oral pigmented lesions might provide a useful index of suspicion for AD in apparently healthy individuals, and thus an adrenocorticotropic hormone (ACTH) stimulation is useful. The spectrum of autoimmune AD comorbidities massively complicates the overall picture of oral manifestations.

Turner syndrome (TS) is characterized by partial or complete loss of a sexual chromosome, resulting in an incomplete development of the body, gonadic failure, cardiac and renal abnormalities, oro-dental changes, etc. In our study, we proposed to perform a histological and immunohistochemical (IHC) study of the periodontium changes in patients with TS. The biological material under study was represented by fragments of gingival mucosa harvested from 18 patients with TS who presented advanced periodontal lesions and required dental extractions. The fragments of gingival mucosa were processed by the classical histological technique of paraffin inclusion, subsequently the obtained sections being stained by the Hematoxylin-Eosin (HE) and examined under the optical microscope. For the IHC study, there were performed serial sections incubated with anti-cluster of differentiation (CD) 3, anti-CD20 and anti-CD68 antibodies for highlighting immune cells, as well as with anti-matrix metalloproteinase (MMP) 2 and anti-MMP8 antibodies for highlighting MMPs (MMP2 and MMP8) involved in the periodontal tissue lesions. In the present study, during the histological examination, there were observed morphological changes, both in the epithelium and in the gingival mucosa chorion. Epithelial changes consisted in the onset of acanthosis processes, in the thickening of the epithelium due to the increase of the spinous layer, as well as in the parakeratosis phenomenon. In the chorion, there was observed the presence of inflammatory infiltrates in various stages, presence of fibrosis (extended in some cases) and the presence of an important vascularization in some cases, with a high number of immunocompetent cells involved in the inborn immune response, but also in the adaptive one, as well as a more or less intense immunoexpression of MMP2 and MMP8. Our study suggests that TS may contribute to the development of some inflammatory processes in the marginal periodontium.

Background/Objectives: Dental caries and gingival inflammation share several biofilm-related determinants. This study evaluated the association between Community Periodontal Index (CPI) screening categories and permanent-dentition caries experience in a consecutively recruited clinical sample of children and adolescents from Southwest Romania. Methods: The multicenter cross-sectional study included 638 participants aged 6–19 years, analyzed as 6–12 years (n = 407) and 13–19 years (n = 231). Analyses included nonparametric comparisons, adjusted Poisson models, a formal CPI-by-age-stratum interaction, continuous-age sensitivity analyses, and generalized Poisson models allowing underdispersion. Results: Mean DMF-T was 4.71 ± 2.55 and 4.93 ± 2.58 in the younger and older strata, respectively. CPI correlated strongly with DMF-T (rho = 0.743 and 0.749; both p < 0.001). Adjusted expected DMF-T counts were higher for CPI 1 and CPI 2 than for CPI 0 in both strata. There was no statistical evidence that the CPI–DMF-T association differed by age stratum (global interaction p = 0.749) or continuous age (p = 0.552). Plaque Index adjustment markedly attenuated CPI estimates; the extent of residual CPI association was sensitive to count-model specification. Conclusions: Higher CPI categories were associated with greater cumulative caries experience in this clinical sample, but the findings do not establish temporality, causality, or predictive validity. Unequal numbers of erupted permanent teeth and CPI-eligible sextants may have contributed to the observed gradient because these quantities were not retained analytically.

Background and Objectives: Caries experience, plaque accumulation, gingival inflammation, and periodontal screening findings may coexist as manifestations of a shared oral-health burden. We examined whether these routinely recorded indicators form distinct multivariable profiles or primarily represent ordered levels along a common burden continuum in children and adolescents. Materials and Methods: This secondary exploratory analysis included 638 participants from a multicenter cross-sectional clinical database: 407 aged 6–12 years and 231 aged 13–19 years. Permanent-dentition Decayed, Missing, and Filled Teeth score, Plaque Index, Gingival Index, and Community Periodontal Index were standardized and analyzed separately by age stratum. Unsupervised K-means clustering compared solutions containing two to five groups to summarize participant-level patterns without imposing predefined clinical categories. Hierarchical Ward classification assessed algorithmic concordance; principal component analysis and a composite standardized burden score assessed dimensionality. Sensitivity analyses excluded the periodontal index or treated it as ordinal with Gower-distance partitioning around medoids, and 1000 repeated 80% subsamples assessed sampling stability using the adjusted Rand index. Results: A single principal component explained 91.0% of variance at 6–12 years and 91.8% at 13–19 years, with all four indicators loading strongly on the same dimension. Ordered cluster membership correlated closely with the composite burden score (Spearman ρ = 0.942 and 0.939; both p < 0.001). The retained low-, intermediate-, and high-burden groupings were highly consistent when the periodontal index was excluded or treated as ordinal and under repeated subsampling. In adolescents, a two-group alternative preserved the low- and high-burden extremes while dividing the intermediate group, indicating that the number of groups changes descriptive granularity rather than revealing a separate phenotype. Conclusions: The principal new finding is that four commonly used oral-health indicators converge on one dominant participant-level burden dimension rather than defining distinct clinical phenotypes. This supports an integrated epidemiological description of cumulative oral-health burden while cautioning against interpreting data-driven groups as diagnostic or treatment categories. The numerical group distributions are sample-specific and require external and longitudinal validation before being transferred to other populations or clinical decision-making.

Background/Objectives: Morphological signs of non-carious tooth surface loss are clinically heterogeneous, and their prevalence depends strongly on the diagnostic framework and threshold used. This exploratory secondary analysis evaluated a study-specific combined morphological outcome restricted to second permanent molars and its association with cumulative caries experience in a regional clinical sample of adolescents. Methods: The analysis included 231 adolescents aged 13–19 years from Dolj, Gorj, and Olt counties, selected from a parent clinical database of 638 participants. The study-specific outcome was coded when a clearly discernible non-carious hard-tissue change compatible with an abrasive, erosive, or abfraction-related morphology was identified on any clinically accessible surface of tooth 17, 27, 37, or 47. This study did not use BEWE, the Smith and Knight Tooth Wear Index, or another validated severity-based tooth wear index; subtype, surface, and severity were not retained separately in the analytical dataset. Dental caries experience was measured using DMF-T. Group comparisons, correlations, and multivariable logistic regression were performed in JASP version 0.96.0. Sensitivity analyses included a participant-level coding audit and a logistic model using DMF-T recalculated after excluding the contribution of teeth 17, 27, 37, and 47. Results: The study-specific morphological outcome was present in 50/231 participants (21.6%). A coding audit confirmed that 181 participants had no positive second molar and 50 had exactly one positive second molar; tooth-specific counts were 14, 15, 12, and 9 for teeth 17, 27, 37, and 47, respectively. In the primary model, male sex (adjusted OR = 3.34, 95% CI 1.67–6.71) and DMF-T (adjusted OR = 1.15 per point, 95% CI 1.01–1.31) were associated with the outcome. After excluding the four evaluated second molars from DMF-T, the caries experience association remained positive but borderline (OR = 1.198, 95% CI 1.000–1.435, p = 0.049), while male sex remained associated (OR = 3.310, 95% CI 1.647–6.652, p < 0.001). Conclusions: A modest exploratory association was observed between the study-specific morphological outcome and cumulative caries experience in this clinical sample. The result should not be interpreted as a standardized NCDL prevalence estimate, a causal relationship, or a prediction model. Confirmation using validated whole-mouth tooth wear measures, outcome-specific reliability assessment, and population-based longitudinal data is required.