Calcified Tissue International最新文献

{"title":"Enamel Tubules and Spindles: Enter and Exit the Amelocyte.","authors":"Alan Boyde, David Mills","doi":"10.1007/s00223-026-01522-w","DOIUrl":"https://doi.org/10.1007/s00223-026-01522-w","url":null,"abstract":"<p><p>By the commonly accepted rules of nomenclature, cells forming hard tissue which become incorporated within the inter- and extra-cellular tissue mass which they secrete are called '-cytes': the spaces in which these cells sit are called lacunae. Hence, osteoblasts become osteocytes in osteocytic lacunae, chondroblasts become chondrocytes, cementoblasts cementocytes, even odontoblasts become odontocytes in some mammalian species. We provide evidence that enamel spindles are cell bodies of ameloblasts which have become entrapped and buried in the enamel matrix produced by the surrounding cells, to produce amelocytic lacunae: it is no life for a cell in a rigid, dense and dead tissue, and we do not suppose that amelocytes live once they are set on that route. Spindles, normally only found at the enamel-dentine junction, are absent when the enamel at the junction is free of prisms, i.e., the ameloblasts had no Tomes' processes. Spindles have an organic content, the amelocyte residue which can be stained - and removed by bleach, after which the spindle space no longer stains. Spindles are extensions of enamel tubules which result from the extension of a fine ameloblastic process [from the major Tomes' process] which unites with an odontoblast process. In marsupial mammals, the spindle-like ends of the enamel tubules are commonly located well within the enamel. Spindles/amelocytes may form at the neonatal line in human deciduous teeth in cases of severe neonatal stress, and these features simply represent encapsulation of moribund ameloblasts. The frequency of spindles at the enamel dentine junction is greater in cases where the tooth germ is severely deformed by growth pressure from the forming root of a neighbouring tooth.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855917","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":"Climate Change and Sarcopenia: Mechanisms, Vulnerabilities, and Public Health Implications.","authors":"Rizwan Qaisar, Firdos Ahmad, Asima Karim","doi":"10.1007/s00223-026-01527-5","DOIUrl":"https://doi.org/10.1007/s00223-026-01527-5","url":null,"abstract":"<p><p>This review explores the emerging relationship between climate change and sarcopenia, a progressive loss of skeletal muscle mass and strength that contributes to frailty and disability in aging populations. It aims to synthesize current evidence on how climate-related stressors may influence muscle health and accelerate sarcopenia onset. We conducted a comprehensive literature review integrating findings from epidemiological studies, mechanistic research, and public health reports. Key climate stressors, including heat stress, air pollution, ultraviolet radiation changes, extreme weather events, and food insecurity, were examined for their biological and environmental impacts on muscle physiology. Vulnerable populations and geographic disparities were also analyzed. Climate stressors impair muscle health through distinct pathways: heat stress activates inflammatory and catabolic signaling; air pollution induces oxidative damage and mitochondrial dysfunction; reduced ultravoilet exposure compromises vitamin D synthesis; and food insecurity limits access to protein and micronutrients. These factors interact with aging physiology, exacerbating muscle decline. Older adults, women, and individuals in tropical, urban, or high-altitude regions are disproportionately affected due to physiological and socioeconomic vulnerabilities. Climate change is a modifiable risk factor for sarcopenia. Integrating environmental indicators into sarcopenia screening, promoting climate-resilient nutrition, and adapting geriatric care systems are essential for mitigating its impact. Interdisciplinary approaches are needed to address the compounded effects of climate stress and aging on muscle health and to inform public health strategies in a warming world.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833844","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":"Impact of Secondhand Smoke on the Biomineralization of Dental Enamel in Rats.","authors":"Juliana de Lima Gonçalves, Alice Corrêa Silva-Sousa, Manoel Damião de Sousa-Neto, Fabrício Kitazono de Carvalho, Alexandra Mussolino de Queiroz, Bernhard Ganss, Francisco Wanderley Garcia de Paula-Silva","doi":"10.1007/s00223-026-01542-6","DOIUrl":"https://doi.org/10.1007/s00223-026-01542-6","url":null,"abstract":"<p><p>This study aims to investigate the qualitative and quantitative morphological changes in dental enamel resulting from SHS exposure during early childhood, utilizing an animal model. Wistar rat offspring were divided into a control group (n = 15) and an SHS exposure group (n = 19). The experimental group was subjected to cigarette smoke twice daily for 5 min, from postnatal day 2 to day 28. Throughout the experimental period, growth was monitored by measuring both weight and body length. Dental enamel was assessed through photographic analysis, micro-computed tomography (micro-CT), scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDS), and microhardness testing. Mandibles were processed, followed by hematoxylin and eosin staining. Data analysis was conducted using Student's t-tests (⍺= 5%). There was a significant reduction in weight gain in the SHS-exposed group compared to controls (p < 0.0001). Macroscopic examination revealed no structural differences in the incisors or molars of SHS-exposed offspring relative to controls. SEM analysis demonstrated increased spacing between superficial enamel prisms was noted in the SHS group. In terms of chemical composition, significant decreases in phosphorus content (p = 0.033) and increases in carbon content (p = 0.017) were detected in the molars of the SHS group, with no significant differences found in calcium, oxygen, or the calcium-to-phosphorus ratio. Micro-CT analysis showed no changes in enamel volume or microhardness, and no significant differences were detected in ameloblast morphology. In conclusion, while SHS exposure did not induce macrostructural changes in enamel, it was associated with reduced phosphorus levels, increased carbon levels, and greater spacing between superficial enamel prisms leading to a mild disturbance in dental mineralization.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834014","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":"Diagnostic Indices for Epidemiological Assessment of Molar Incisor Hypomineralization: A Systematic Review.","authors":"Marta Mazur, Artnora Ndokaj, Marta Berdzik-Janecka, Irena Dus-Ilnicka, Roman Ardan, Sylvie Babajko, Katia Jedeon","doi":"10.1007/s00223-026-01538-2","DOIUrl":"https://doi.org/10.1007/s00223-026-01538-2","url":null,"abstract":"<p><p>Molar incisor hypomineralization (MIH) is a qualitative developmental defect of enamel and one of the most prevalent oral health conditions in childhood. Over the last two decades, increasing attention has been given to its prevalence and etiology; however, marked heterogeneity in diagnostic criteria and indices has limited the comparability of epidemiological findings. This systematic review aimed to identify and describe the diagnostic indices used for the epidemiological assessment of MIH in the general pediatric population. A systematic literature search was conducted in PubMed, Scopus, and Google Scholar to identify epidemiological studies published between January 2001 and December 2024 reporting MIH prevalence in children. Study selection, data extraction, and methodological quality assessment were performed independently by two reviewers in accordance with PRISMA guidelines. The review protocol was registered in PROSPERO (CRD42022345224). A total of 198 articles were included, corresponding to 201 independent epidemiological studies, as three articles reported results from two distinct study populations. The European Academy of Paediatric Dentistry (EAPD) criteria were used in 171 studies (75.7%), representing the most widely adopted diagnostic index. Other indices, including the modified Developmental Defects of Enamel index (mDDE), Mathu-Muju and Wright, Wetzel and Reckel, MIH Severity Scoring System (MIH-SSS), the MIH Treatment Need Index (MIH TNI) criteria, and FDI criteria, were used infrequently. Studies using EAPD criteria accounted for the largest cumulative sample size and showed a descriptively aggregated MIH prevalence of 12.9%, whereas prevalence estimates varied across alternative diagnostic indices. In conclusion, the lack of uniform diagnostic standards and nomenclature hampers global surveillance and limits the comparability of prevalence data. The adoption of MIH-specific diagnostic criteria, supported by adequate examiner calibration and transparent reporting, is essential to improve the quality, consistency, and interpretability of future epidemiological research.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834047","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":"Preserved Mandibular Bone Microarchitecture Following Ovariectomy-induced Osteoporosis is Associated with a Specific Fatty Acid Composition in the Rat.","authors":"Maxime Bedez, Nicolas Bertheaume, Jérôme Delattre, Cécile Olejnik, Alexandrine During","doi":"10.1007/s00223-026-01543-5","DOIUrl":"https://doi.org/10.1007/s00223-026-01543-5","url":null,"abstract":"","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834140","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":"Pre-eruptive Coronal Resorptions as a Clinical Feature of FAM83H-Related Amelogenesis Imperfecta: Insights from Two Brazilian Families.","authors":"Kemelly Karolliny Resende, Luanna de Sousa Amorim, Lilian Marly de Paula, André Ferreira Leite, Juliana Forte Mazzeu, Paulo Marcio Yamaguti, Ana Carolina Acevedo","doi":"10.1007/s00223-026-01540-8","DOIUrl":"10.1007/s00223-026-01540-8","url":null,"abstract":"<p><p>Amelogenesis Imperfecta (AI) is a group of rare hereditary conditions characterized by quantitative and/or qualitative enamel defects affecting both primary and permanent dentitions. Among the more than 70 genes associated with AI, FAM83H is the only gene known to cause autosomal dominant hypocalcified AI (ADHCAI). Recent studies have shown that causative variants in FAM83H disrupt amelogenesis and may also affect dental follicle cells, potentially leading to tooth impaction in ADHCAI patients. Here, we report two unrelated Brazilian patients with ADHCAI who present a distinctive and severe phenotype characterized by delayed eruption, multiple impacted teeth, and pre-eruptive crown resorptions (PECR). Longitudinal radiographic analysis revealed multiple unerupted teeth with progressive PECR. Using whole-exome sequencing, we identified two nonsense heterozygous FAM83H causative variants (c.1055 C > A, p.Ser352*; c.1379G > A, p.Trp460*). Our findings represent the first report of FAM83H-related ADHCAI in Brazilian families and expand both the phenotypic spectrum and clinical severity associated with this gene. The presence of widespread PECR and adjacent bone alterations suggests that FAM83H dysfunction may affect not only enamel formation but also tooth eruption pathways and local tooth-bone interactions. This study highlights the importance of early diagnosis, individualized radiographic follow-up, and genetic testing to guide counselling and clinical management of affected individuals.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811150","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 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":3.2,"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":"https://doi.org/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":3.2,"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":3.2,"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":"https://doi.org/10.1007/s00223-026-01526-6","url":null,"abstract":"","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"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}