Calcified Tissue International最新文献

{"title":"The Role of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) in Enamel Formation.","authors":"Jake Ngu, Charles M Met, Atoosa Heidari Bigvand, Yan Zhang, Pamela K Den Besten","doi":"10.1007/s00223-026-01539-1","DOIUrl":"10.1007/s00223-026-01539-1","url":null,"abstract":"<p><p>Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis (CF), an autosomal recessive multiorgan disorder. In addition to respiratory, digestive, and reproductive pathologies, patients with CF also exhibit higher rates of enamel defects. CFTR is an anion channel expressed in maturation-stage ameloblasts and is known for its role in chloride and bicarbonate conductance, a function thought to promote enamel mineralization through the neutralization of protons released during hydroxyapatite formation. Previous studies of CFTR global knockout mice have shown hypomineralization and acidification of the maturation-stage enamel matrix. However, the systemic nature of CF and the contribution of extrinsic factors may contribute to these findings. To determine how CFTR specifically contributes to amelogenesis, we generated a conditional knockout mouse in which CFTR loss-of-function is driven by Cre expression under the promoter of the maturation-stage ameloblast marker, Odam. CFTR loss-of-function resulted in the formation of hypomineralized enamel. The enamel matrix was acidified, and loss of matrix pH cycling coincided with arrested ameloblast modulation as indicated by failed re-localization of tight/ gap junctions and ion transporters to the ameloblast distal membrane. Amelogenin hydrolysis was reduced and retained in the maturing enamel matrix, which was associated with reduced Klk4 expression and activity. Transcriptional analyses of incisor ameloblasts showed reduced expression of acid-base regulators, consistent with dysregulation of both intracellular and extracellular pH. Together, these findings show multiple functions of CFTR in incisor enamel maturation, including regulation of intra/ extracellular pH, ameloblast modulation, and extracellular matrix remodeling.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dissecting Immune Mechanisms Underlying Sarcopenia Using Multi-omics Approaches.","authors":"Kaixi Ding, Wei Jiang, Ming Lei, Yongxiang Gao","doi":"10.1007/s00223-026-01524-8","DOIUrl":"10.1007/s00223-026-01524-8","url":null,"abstract":"<p><p>Sarcopenia is an age-related muscle disease, and its gene regulation in immune cells is not well understood. Using immune cell-specific single-cell expression quantitative trait loci (sc-eQTLs), genome-wide association studies (GWAS), and multi-omics data, we systematically explored their potential causal roles in sarcopenia. We integrated sc-eQTL and cis-eQTL data from whole blood and skeletal muscle, seven sarcopenia-related phenotypes GWAS summary statistics, and used a Muscle Function-Mass Genetic Structural Equation Model (MF-M GSEM), Mendelian randomization (MR), and Bayesian colocalization analyses to assess causal gene effects across 14 immune cell types, whole blood, and skeletal muscle. A two-step MR was then applied to explore mediation through common diseases and carnitine-related metabolites. Fourteen genes, including HLA-DRB1, HLA-C, and SLC22A5, showed significant causal effects on at least three sarcopenia phenotypes in one or more immune cell types (Bonferroni-adjusted P < 0.05; posterior probability for hypothesis 4 > 0.8). Heart failure, rheumatoid arthritis, and chronic kidney disease mediated the causal effects of sc-eQTLs for FNBP4, HLA-DRB1, HLA-C, and HLA-DQA1 on MF-M GSEM (P < 0.05). Isovalerylcarnitine (C5) mediated the causal effect of the cis-eQTL of SLC22A5 in skeletal muscle on MF-M GSEM, with a mediation proportion of 67.6% (FDR-adjusted P < 0.05). Our findings highlight that immune cell-specific expression of HLA-DRB1, HLA-C, SLC22A5, and FNBP4 contributes to the pathogenesis of sarcopenia, suggesting these genes as potential therapeutic targets and mechanistic entry points for future research.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating α-Klotho and Multidimensional Aging and Frailty Outcomes: A Systematic Review and Meta-Analysis from the European Renal Association CKD-MBD Working Group.","authors":"Mustafa Guldan, Lasin Ozbek, Derya G Fidan, Arif E Narin, Ditte Hansen, Juan M Diaz-Tocados, Mathias Haarhaus, Martin H de Borst, Carlo Alfieri, Pietro M Ferraro, Antonio Bellasi, Mehmet Kanbay","doi":"10.1007/s00223-026-01537-3","DOIUrl":"10.1007/s00223-026-01537-3","url":null,"abstract":"<p><p>Although α-Klotho has gained attention as a promising biomarker of aging, its association with frailty and broader aging-related outcomes beyond chronic kidney disease-mineral and bone disorder remains incompletely characterized. This systematic review and meta-analysis aimed to investigate the association between circulating α-Klotho levels and aging-related outcomes, including frailty, effects of physical activity and exercise interventions, body composition, cognitive and neuropsychiatric status, sarcopenia, and bone mineral density (BMD). A comprehensive literature search was performed across multiple electronic databases, including Ovid MEDLINE, Web of Science, Scopus, PubMed, and the Cochrane Library, to identify relevant studies published up to April 30, 2025. Pooled analyses were conducted using random-effects models, with effect estimates synthesized as mean differences, odds ratios, or correlation coefficients, and heterogeneity assessed using the I² statistic. Risk of bias was assessed using design-specific tools, including the Newcastle-Ottawa Scale, the Risk of Bias 2 tool (RoB2) of the Cochrane collaboration, and the Joanna Briggs Institute (JBI) checklists. A total of 109 studies met the inclusion criteria and were included. In our meta-analysis, higher circulating α-Klotho levels were significantly associated with lower odds of frailty (OR = 0.61, 95% CI: 0.49, 0.77; p < 0.0001, I² = 0%). Exercise interventions increased circulating α-Klotho (95% CI: 93.93, 261.73, p < 0.0001; I² = 89%), but habitual physical activity showed no significant effect on α-Klotho compared to inactive controls (p = 0.25; I² = 100%). Lower circulating α-Klotho levels were observed in individuals with osteoporosis compared with those with normal BMD (95% CI: - 114.98, - 25.49; p = 0.002) and in individuals with osteopenia compared with those with normal BMD (95% CI: - 123.22, - 0.74; p = 0.05), and were associated with fractures. Based on qualitative synthesis, circulating α-Klotho levels were positively associated with multiple physical function outcomes, including grip strength, short physical performance battery scores, and sit-to-stand performance, with mixed findings for gait speed and the 6-min walk test. Circulating α-Klotho appears to be a promising biomarker for frailty, physical function, and bone health in aging; however, evidence for cognitive outcomes remains limited and inconsistent. Substantial heterogeneity and the observational nature of most studies highlight the need for more standardized and longitudinal research.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13132909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Plastin in Bone, Cartilage, and Related Diseases.","authors":"Zuping Wu, Hengyuan Liu, Ruifeng Song, Siyu Chen, Jiejun Shi, Xiaoxia Feng, Qian Chen","doi":"10.1007/s00223-026-01526-6","DOIUrl":"10.1007/s00223-026-01526-6","url":null,"abstract":"<p><p>The plastin family (PLS1, PLS2, PLS3) comprises highly conserved actin-binding proteins (ABPs) that regulate cytoskeletal dynamics by cross-linking actin microfilaments and play key roles in bone and cartilage development, homeostasis, and disease. PLS1 primarily stabilizes tight actin bundles in epithelial brush-border microvilli and has also been reported to support osteoblast differentiation via regulating intracellular Ca2+ homeostasis. In bone, PLS3 mutations lead to X-linked osteoporosis through mechanisms involving the inhibition of the WNT pathway, activation of TH17 cell differentiation, and disorders of osteogenesis mediated by the neutrophil extracellular trap (NET) pathway. Meanwhile, PLS2 promotes osteoclast sealing ring assembly and drives bone resorption via Ser-5/Ser-7 phosphorylation. In cartilage, PLS3 is highly expressed on the surface layer of osteoarthritis (OA) patients, with expression levels positively correlating with degeneration severity, possibly involved in chondrocyte hypertrophy in response to mechanical loading. Pathologically, PLS3 deficiency directly causes early-onset osteoporosis and increased fracture risk, while PLS2 plays a dual role in cancer metastasis and inflammation. Targeting plastin, such as inhibiting PLS2 phosphorylation or supplementing PLS3 mRNA, offers potential new strategies for treating hyperresorption and hereditary bone diseases.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impaired Remodeling of Tight Junctions Associated with Loss of Enamel Rod Decussation in Tgfbr2^G357W/+ Mice.","authors":"Olivier Duverger, Valentina Baena, Zulfeqhar A Syed, Janice S Lee","doi":"10.1007/s00223-026-01541-7","DOIUrl":"10.1007/s00223-026-01541-7","url":null,"abstract":"<p><p>During enamel secretion, ameloblasts follow a complex coordinated movement that results in the enamel rods being arranged in a crisscross pattern that contributes significantly to its exceptional mechanical properties. We previously determined that mutations in the gene encoding TGF-β receptor 2 (TGFR-2) in humans (TGFBR2) and mice (Tgfbr2) result in the formation of fully mineralized enamel that exhibits impaired decussation of enamel rods. Using Tgfbr2^G357W/+ mice, we demonstrated that this phenotype was due to disrupted coordinated movement of ameloblasts during enamel secretion. In this study, we used focused ion beam scanning electron microscopy (FIB-SEM) to look more closely at the area of the apical terminal web (ATW) where the cells are connected via tight junctions. We show that ameloblasts from wild-type littermates exhibit an abrupt shift in orientation at the ATW while Tgfbr2^G357W/+ mice show no signs of such shift. Moreover, ZO-1 distribution at the ATW was abnormal in Tgfbr2^G357W/+ mice with reduced accumulation at the ATW and presence of clusters of the protein at the basal side. These results suggest that abrupt orientation shift at the ATW via dynamic remodeling of tight junctions is essential for rows of ameloblasts to deposit enamel rods in opposite directions.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13132921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amelogenin Phosphorylation Affects Protein-Protein Interactions In Vivo.","authors":"Brent Vasquez, Ai Thu Bui, Henry C Margolis, Elia Beniash","doi":"10.1007/s00223-026-01530-w","DOIUrl":"10.1007/s00223-026-01530-w","url":null,"abstract":"<p><p>Amelogenin (AMELX), the predominant extracellular matrix protein (EMP) in forming enamel, has a single phosphorylation site at Serine 16 (S16). Previously, we demonstrated that AMELX phosphorylation enhances its ability to stabilize amorphous calcium phosphate and inhibit mineralization. To study the role of AMELX phosphorylation in vivo, we substituted S16 with Ala to prevent phosphorylation in a generated AmelxS16A knock-in (KI) mice. These KI mice exhibited hypoplastic enamel with ectopic calcifications, a lack of enamel rods, an accelerated transformation of amorphous calcium phosphate (ACP) to apatitic enamel crystals, and progressive pathological changes in ameloblasts, the enamel forming cells responsible for enamel production. The goal of this study was to test the hypothesis that the phosphorylation status of AMELX affects its interactions with other proteins in the extracellular enamel space. To determine the effect of AMELX phosphorylation on the protein–protein interactions, we have conducted Proximity Ligation Assays (PLA) of wild type (WT) and KI mandibular incisors. Specifically, we conducted PLA of Amelx with a transmembrane acid phosphatase 4 (Acp4), basal lamina protein laminin β3 (Lamβ3) and the EMP ameloblastin (Ambn). Quantitative image analysis showed significantly higher PLA signal for Acp4 in the ameloblast cell bodies and distal ends of WT mice. PLA signal was also significantly higher for Ambn in the ameloblast distal ends and in the enamel matrix of WT mice. For Lam5, the signal was also higher in ameloblasts cell bodies, ameloblast distal ends and the enamel matrix of WT mice. Collectively, the significantly higher PLA signals between phosphorylated Amelx and Ambn, Acp4, and Lamβ3, compared with nonphosphorylated Amelx, suggest that AMELX phosphorylation promotes potentially important protein–protein interactions during amelogenesis.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13333156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Life Microplastic Exposure Impairs Mouse Incisor Enamel Formation.","authors":"Yiting Li, Jiahui Zheng, Sihan Yu, Qingquan Shi, Mian Wan, Liwei Zheng","doi":"10.1007/s00223-026-01535-5","DOIUrl":"10.1007/s00223-026-01535-5","url":null,"abstract":"<p><p>Microplastics (MPs) are pervasive environmental contaminants with growing evidence of systemic toxicity; however, their effects on tooth development during early life remain poorly understood. In the present study, we investigated whether early-life exposure to polystyrene microplastics (PS-MPs) affects tooth eruption, root formation, and enamel development in mice. Pregnant mice were administered 1, 4, and 10 μm PS-MPs (10 μg/kg/day) from gestation through lactation, and offspring continued exposure post-weaning. Mandibles were analyzed at postnatal days 14, 25, and 42 using micro-computed tomography, histology, scanning electron microscopy, and microhardness testing. Early-life MP exposure did not affect maternal outcomes or overall offspring growth. However, it significantly delayed molar eruption and root formation and produced incisor enamel defects, including reduced enamel length and volume, decreased mineral density, and decreased mechanical hardness. These effects exhibited particle size dependency, with 1 μm MPs causing the most significant changes. Histological analyses revealed increased proliferation of transit-amplifying cells in the labial cervical loop and postponed ameloblastic differentiation, accompanied by an incisal shift in enamel matrix deposition. Collectively, these findings demonstrate that early-life MP exposure disrupts tooth development in a size-dependent manner and identify developing dental tissues as sensitive targets of environmental MP exposure.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serine-16 Phosphorylation, C-Terminal Truncation, and Ion-Specific Interactions Coordinate Amelogenin Nanoribbon Formation.","authors":"Emerson Tavares de Sousa, Johan Svensson Bonde, Kevin Lu, Yushi Bai, Stefan Habelitz","doi":"10.1007/s00223-026-01505-x","DOIUrl":"10.1007/s00223-026-01505-x","url":null,"abstract":"<p><p>Amelogenin self-assembly is a critical step in enamel matrix organization, supporting the spatial confinement of transient ACP and orchestrating hydroxyapatite nucleation and ordered growth. Studies have demonstrated that amelogenin self-assembles into nanoribbons by forming an amyloid-like structure that matches the cross-β pattern observed in the developing enamel matrix. However, molecular determinants remain unclear. In this work, we demonstrate that Ser16 phosphorylation (pS16) and Mmp20-mediated C-terminal truncation exert complementary control over amelogenin self-assembly and templated mineralization. Using advanced microscopy and spectroscopic methods, we show that C-terminal truncation lowers the energetic threshold for the disordered-to-ordered β-sheet phase transformation, producing rapid nanoribbon growth, whereas pS16 prolongs this transformation barrier and channels assembly into a gradual, more orderly templating process. Remarkably, pS16 alone is sufficient to drive nanoribbon formation under ion-free conditions, facilitating ion-mediated charge compensation at the self-assembly N-terminal domain that otherwise requires calcium and phosphate ions. These ions play complementary roles: phosphate appears to promote longitudinal elongation through interactions with protonated His-rich motifs, whereas calcium strengthens lateral cohesion and bundling by binding acidic C-terminal residues and engaging with the pS16 site, which could also foster ACP accumulation along the nanoribbon central zone. In a revised structural model, this central zone likely represents a longitudinal interface between two strands of beta-sheets, forming a steric-zipper by interactions of isoleucine and phenylalanine. Together, these results establish a framework in which pS16, C-terminal truncation, and ion-specific interactions cooperate to fine-tune amelogenin self-assembly and direct ribbon-like mineral formation in enamel.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13340613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-Specific Associations of Radiographic Knee Osteoarthritis and Pain with Distal Tibia Bone Microarchitecture: the Study of Muscle, Mobility and Aging (SOMMA).","authors":"Tong Yu, Andy Kin On Wong, Nina Z Heilmann, Kerri S Freeland, Bradley C Nindl, Kristen J Koltun, Andrew J Burghardt, Julie M Hughes, Peggy M Cawthon, Jane A Cauley, Elsa S Strotmeyer, Nancy E Lane","doi":"10.1007/s00223-026-01531-9","DOIUrl":"10.1007/s00223-026-01531-9","url":null,"abstract":"<p><p>Knee osteoarthritis (OA) is the most common joint disease and despite being associated with higher areal bone mineral density (aBMD), increases fracture risk. This paradox suggests that in addition to mobility and fall concerns, microarchitectural deficits, not captured by DXA, may contribute to skeletal fragility in knee OA. This study aimed to examine cross-sectional associations of radiographic knee OA and knee pain with bone microarchitecture at the distal tibia and distal radius, assessed by high-resolution peripheral quantitative computed tomography (HR-pQCT), in older adults. We studied 107 men and 159 women (age 77 ± 5 years) from the study of muscle, mobility and aging (SOMMA) who had knee radiographs and HR-pQCT scans. Radiographic knee OA was defined as Kellgren–Lawrence grade (KLG) 3–4, and knee pain was assessed using the Brief Pain Inventory questionnaire. Linear regression models estimated sex-specific associations of knee OA and pain with standardized HR-pQCT parameters, adjusting for age, BMI, FN aBMD, physical activity, fracture history, smoking, alcohol, and medication use. In women, at the distal tibia, radiographic knee OA was associated with lower cortical vBMD (B = − 0.55 SD, 95% CI − 0.91, − 0.20). In men, knee pain was associated with lower total and cortical vBMD, thinner cortices, and larger trabecular area. No associations were detected at the distal radius. Radiographic knee OA was more strongly associated with lower distal tibia cortical density in women, while pain was associated with overall structural and density deficits at distal tibia in men. These sex-specific patterns may inform fracture risk and OA etiology.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111493/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Micro-Raman Spectroscopy Reveals Compositional Alterations in Molar Incisor Hypomineralization and Enamel Adjacent to Demarcated Opacities.","authors":"Flaureta Rexhaj, Furqan A Shah, Ted Lundgren","doi":"10.1007/s00223-026-01517-7","DOIUrl":"10.1007/s00223-026-01517-7","url":null,"abstract":"<p><p>Molar incisor hypomineralization (MIH) is a developmental condition that impairs enamel mineralization in the first permanent molars and often the permanent incisors. Clinically, MIH presents as demarcated opacities, ranging from white–yellow discolorations in mild cases to yellow–brown discolorations with enamel breakdown in severe cases. The longevity of direct adhesive restorations depends on reliable bonding to sound enamel, and current clinical practice involves removing visibly affected enamel and bonding adhesive restorations to apparently sound tissue. Accurately identifying healthy enamel is therefore crucial. Despite increasing recognition of MIH, there remains a gap in understanding its pathogenesis and the optimal treatment strategies needed to ensure long-term restorative success. The enamel adjacent to demarcated opacities has not been thoroughly investigated, raising a critical question: does visually translucent, seemingly intact enamel next to MIH opacities truly represent unaffected tissue? This work uses micro-Raman spectroscopy to determine whether chemical and structural alterations extend beyond the margins of demarcated opacities into adjacent translucent enamel. The findings indicate that MIH involves not only the visibly opaque enamel but also the adjacent translucent enamel, which shows increased fluorescence, lower mineral crystallinity, and elevated acid phosphate and carbonate content. These substitutions are consistent with a more soluble and porous apatite phase that is less chemically durable in the physiological environment. The adjacent translucent region consistently occupies an intermediate position between healthy controls and opacities, supporting its classification as affected tissue, and highlighting implications for adhesive strategies, margin placement, and preventive management of MIH-affected teeth.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}