{"title":"Association of Sweetened Beverages with Risk of Osteoporosis and First Fractures: Evidence from the United Kingdom Biobank.","authors":"Ji-Eun Youn, Yu-Jin Kwon, Yae-Ji Lee, Tae-Hwa Han, Seok-Jae Heo, Ji-Won Lee","doi":"10.1007/s00223-026-01506-w","DOIUrl":"https://doi.org/10.1007/s00223-026-01506-w","url":null,"abstract":"<p><p>We investigated the associations between intake of sugar-sweetened, artificially sweetened, and naturally sweetened beverages (SSBs, ASBs, and NSBs) and osteoporosis and first incident fracture risks. We analyzed data from 171,694 to 168,366 United Kingdom Biobank participants (mean age: 55.8 ± 7.96 years; 53.9% and 52.9% women, respectively) for osteoporosis and fracture outcomes. Median follow-up durations were 13.5 and 13.4 years, respectively. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). High ASB intake (> 1 serving/day) was associated with increased osteoporosis (HR, 1.29 [95% CI 1.14-1.47]) and fracture risk (HR: 1.11; 95% CI 1.01-1.22]). Moderate NSB intake (> 0-1 serving/day) was associated with reduced osteoporosis risk (HR: 0.88; 95% CI 0.83-0.93), particularly among individuals aged < 60 years (HR: 0.84; 95% CI 0.78-0.91). Among women, moderate NSB intake was protective (HR: 0.86; 95% CI 0.80-0.92), whereas among men, higher intake (> 1 serving/day) showed benefits (HR: 0.72; 95% CI 0.54-0.97). Among participants with hypertension, high NSB intake was linked to increased incident fracture risks (HR: 1.23; 95% CI 1.05-1.44). Moderate SSB intake was associated with slightly decreased incident fracture risks (HR: 0.92; 95% CI 0.88-0.97), whereas higher intake was not significantly associated. High ASB intake correlated with increased osteoporosis and fracture risks. Conversely, moderate NSB intake appeared protective, particularly in younger individuals and women. These findings highlight that beverage type, quantity, and individual characteristics may influence bone health.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763097","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":"Tetracycline Enables Visualization of Remineralization Induced by Agents Penetrating Dental Enamel.","authors":"Alexis Murat, Katia Jedeon, Anne-Lyse Denizot, Charlotte Duval, Gilles Richard, Sylvie Babajko, Sophia Houari","doi":"10.1007/s00223-026-01503-z","DOIUrl":"https://doi.org/10.1007/s00223-026-01503-z","url":null,"abstract":"<p><p>The demineralization of tooth enamel caused by acid attack in dental biofilms is a significant challenge in dentistry. While fluoride varnishes are widely used to protect and restore the enamel surface, their actual ability to penetrate and treat the enamel in depth remains poorly understood. This study proposes an innovative in vitro approach to visualize the diffusion of remineralizing agents into enamel depth using by confocal laser scanning microscopy (CLSM). Four commercial fluoride varnishes (MI Varnish<sup>®</sup>, Duraphat<sup>®</sup>, FluoroCal<sup>®</sup>, Clinpro Clear Fluoride<sup>®</sup>) were applied to artificially demineralized bovine enamel samples in the presence of tetracycline. We used the tetracycline's properties to bind to calcium and form a fluorescent complex to track the remineralization activity of varnishes. The results demonstrate the absence of autofluorescence in the controls and the presence of a specific fluorescent emission for the active varnishes. MI Varnish<sup>®</sup> demonstrated the most significant penetration in enamel depth (42.0 ± 11.6 μm), followed by Duraphat<sup>®</sup>, FluoroCal<sup>®</sup>, and Clinpro Clear Fluoride<sup>®</sup>. This non-destructive method provides accurate three-dimensional visualization of remineralized areas and is a promising tool for evaluating fluoride varnishes effectiveness.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13102789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763425","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}
Lu Liu, Cheuk Wang Au, Ummey Hany, Alice L Rigby, Anesha Chauhan, Catriona Brown, Jessie Sims, Gina Murillo, Marìa Gabriela Acosta de Carmargo, Chris F Inglehearn, Christopher M Watson, Alan J Mighell, Claire E L Smith
{"title":"ACP4 Variants in Hypoplastic Amelogenesis Imperfecta.","authors":"Lu Liu, Cheuk Wang Au, Ummey Hany, Alice L Rigby, Anesha Chauhan, Catriona Brown, Jessie Sims, Gina Murillo, Marìa Gabriela Acosta de Carmargo, Chris F Inglehearn, Christopher M Watson, Alan J Mighell, Claire E L Smith","doi":"10.1007/s00223-026-01512-y","DOIUrl":"10.1007/s00223-026-01512-y","url":null,"abstract":"<p><p>Amelogenesis imperfecta (AI) is a group of rare inherited conditions causing tooth enamel defects. Human acid phosphatase 4 (ACP4) is a transmembrane protein involved in maintaining appositional enamel growth. Variants in ACP4 cause recessive hypoplastic AI. Here we identify further families and review published ACP4 variants causing AI. In three Pakistani families, we identified a new ACP4 variant, c.254T > C, p.(Pro85Leu), which long-read sequencing revealed to be a founder variant. Two further families were homozygous for previously reported pathogenic ACP4 variants. Further details are also reported for two families previously listed in a technical/cohort study by this group. In total, seventeen ACP4 variants had been reported in the literature causing AI in seventeen families prior to this study. This report adds an eighteenth variant and brings the total to 22 families. Nine families derive from a cohort of over 400 AI probands curated in Leeds, UK, and account for 9/129 families solved for recessive AI, suggesting ACP4 variants are a significant cause of recessive AI. ACP4 variants implicated in AI include fifteen missense, one splice and two frame-breaking deletions. Most missense variants are within the acid phosphatase domain, with one in the transmembrane domain. The consistent hypoplastic phenotype suggests a single mutational mechanism, and the report of a family with a homozygous frameshift variant likely to be subject to nonsense mediated decay points to loss of function. Missense variants alter amino acids at the catalytic core or affect protein stability, homodimerisation or membrane localisation, all likely to result in functional insufficiency.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13070050/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662279","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}
Hennie G Raterman, Giovanni Adami, Patricia Clark, Glenn Haugeberg, Jorge Morales Torres, Luis Vidal Neira, Leith Zakraoui, Cristiano Zerbini, Osvaldo D Messina, Willem F Lems
{"title":"Osteoimmunology: Can We Prevent Bone Loss in Rheumatoid Arthritis with Modern Antirheumatic Drugs?","authors":"Hennie G Raterman, Giovanni Adami, Patricia Clark, Glenn Haugeberg, Jorge Morales Torres, Luis Vidal Neira, Leith Zakraoui, Cristiano Zerbini, Osvaldo D Messina, Willem F Lems","doi":"10.1007/s00223-026-01504-y","DOIUrl":"https://doi.org/10.1007/s00223-026-01504-y","url":null,"abstract":"","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662293","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}
Babajko Sylvie, Buzalaf Marilia, Fini Jean-Baptiste, Den Besten Pamela
{"title":"Water Fluoridation Risks or Benefits: Summary of the Symposium Presented During the Enamel 11 Meeting Held in Paris France.","authors":"Babajko Sylvie, Buzalaf Marilia, Fini Jean-Baptiste, Den Besten Pamela","doi":"10.1007/s00223-026-01525-7","DOIUrl":"https://doi.org/10.1007/s00223-026-01525-7","url":null,"abstract":"","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662309","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}
Pauliina Utriainen, Markus A Hartmann, Stéphane Blouin, Takolander Sofia, Outi Mäkitie, Nadja Fratzl-Zelman
{"title":"Low Bone Turnover and Decreased Bone Matrix Mineralization at Diagnosis in Children with Acute Lymphoblastic Leukemia.","authors":"Pauliina Utriainen, Markus A Hartmann, Stéphane Blouin, Takolander Sofia, Outi Mäkitie, Nadja Fratzl-Zelman","doi":"10.1007/s00223-026-01509-7","DOIUrl":"10.1007/s00223-026-01509-7","url":null,"abstract":"","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13046658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590366","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}
J Tostes-Figueiredo, N Macedo-Ribeiro, G H L Santos, I M Porto, R F Gerlach, F B de Sousa
{"title":"Effects of fluoride and lead on enamel composition during the maturation stage of amelogenesis in rat mandibular third molars.","authors":"J Tostes-Figueiredo, N Macedo-Ribeiro, G H L Santos, I M Porto, R F Gerlach, F B de Sousa","doi":"10.1007/s00223-026-01511-z","DOIUrl":"10.1007/s00223-026-01511-z","url":null,"abstract":"","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13046661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590315","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}
Claes Ohlsson, Anna E Törnqvist, Karin H Nilsson, Maria Nethander, Jianyao Wu, Lei Li, Antti Koskela, Sofia Movérare-Skrtic
{"title":"Role of Complement Component 9 in Bone Health: Causal Evidence in Humans and Mechanistic Studies in Mice.","authors":"Claes Ohlsson, Anna E Törnqvist, Karin H Nilsson, Maria Nethander, Jianyao Wu, Lei Li, Antti Koskela, Sofia Movérare-Skrtic","doi":"10.1007/s00223-026-01515-9","DOIUrl":"10.1007/s00223-026-01515-9","url":null,"abstract":"<p><p>Complement component 9 (C9) is the main pore-forming protein of the terminal membrane attack complex (MAC) in the complement system. The MAC forms a lytic pore in the membrane of target cells and is a key effector of the innate immune system. Excessive complement activation has been implicated in chronic inflammation, which is a well-established risk factor for increased fracture susceptibility. Although other components of the complement system have been linked to bone mass regulation, the role of C9 is unknown. The aim of the present study was to determine the role of C9 for bone health. To determine the role of circulating, mainly liver-derived, C9 in humans, we conducted Mendelian randomization (MR) using a single-SNP instrument and performed genetic colocalization analyses. Genetically predicted higher circulating C9 levels were causally associated with increased risk of forearm fractures and fractures at any bone site. Colocalization analyses supported these findings. Mechanistic studies were performed in mice. As expected, high C9 expression was observed in the liver, while the expression was low in cortical bone and no expression was observed in trabecular bone. Adult female mice with global C9 deletion (C9<sup>-/-</sup>) exhibited lower vertebral trabecular bone volume fraction due to a decreased trabecular number, but they were partly protected against ovariectomy-induced trabecular bone loss. No skeletal phenotype was observed in the femur or in male C9<sup>-/-</sup> mice. In conclusion, high genetically determined circulating C9 is causally linked to increased fracture risk in humans. In mice, global inactivation of C9<sup>-/-</sup> affects vertebral trabecular bone in a sex-specific and context-dependent manner.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13046653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590297","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}