X-linked hypophosphataemia (XLH) is the most common cause of inherited phosphate wasting and is associated with severe complications such as rickets, lower limb deformities, pain, poor mineralization ...of the teeth and disproportionate short stature in children as well as hyperparathyroidism, osteomalacia, enthesopathies, osteoarthritis and pseudofractures in adults. The characteristics and severity of XLH vary between patients. Because of its rarity, the diagnosis and specific treatment of XLH are frequently delayed, which has a detrimental effect on patient outcomes. In this Evidence-Based Guideline, we recommend that the diagnosis of XLH is based on signs of rickets and/or osteomalacia in association with hypophosphataemia and renal phosphate wasting in the absence of vitamin D or calcium deficiency. Whenever possible, the diagnosis should be confirmed by molecular genetic analysis or measurement of levels of fibroblast growth factor 23 (FGF23) before treatment. Owing to the multisystemic nature of the disease, patients should be seen regularly by multidisciplinary teams organized by a metabolic bone disease expert. In this article, we summarize the current evidence and provide recommendations on features of the disease, including new treatment modalities, to improve knowledge and provide guidance for diagnosis and multidisciplinary care.
The major mineralized tissues are bone and teeth, which share several mechanisms governing their development and mineralization. This crossover includes the hormones that regulate circulating calcium ...and phosphate concentrations, and the genes that regulate the differentiation and transdifferentiation of cells. In developing endochondral bone and in developing teeth, parathyroid hormone-related protein (PTHrP) acts in chondrocytes to delay terminal differentiation, thereby increasing the pool of precursor cells. Chondrocytes and (in specific circumstances) pre-odontoblasts can also transdifferentiate into osteoblasts. Moreover, bone and teeth share outcomes when affected by systemic disorders of mineral homeostasis or of the extracellular matrix, and by adverse effects of treatments such as bisphosphonates and fluoride. Unlike bone, teeth have more permanent effects from systemic disorders because they are not remodelled after they are formed. This Review discusses the normal processes of bone and tooth development, followed by disorders that have effects on both bone and teeth, versus disorders that have effects in one without affecting the other. The takeaway message is that bone specialists should know when to screen for dental disorders, just as dental specialists should recognize when a tooth disorder should raise suspicions about a possible underlying bone disorder.
Dentin organic matrix, with type I collagen as the main component, is exposed after demineralization in dentinal caries, erosion or acidic conditioning during adhesive composite restorative ...treatment. This exposed matrix is prone to slow hydrolytic degradation by host collagenolytic enzymes, matrix metalloproteinases (MMPs) and cysteine cathepsins. Here we review the recent findings demonstrating that inhibition of salivary or dentin endogenous collagenolytic enzymes may provide preventive means against progression of caries or erosion, just as they have been shown to retain the integrity and improve the longevity of resin composite filling bonding to dentin. This paper also presents the case that the organic matrix in caries-affected dentin may not be preserved as intact as previously considered. In partially demineralized dentin, MMPs and cysteine cathepsins with the ability to cleave off the terminal non-helical ends of collagen molecules (telopeptides) may lead to the gradual loss of intramolecular gap areas. This would seriously compromise the matrix ability for intrafibrillar remineralization, which is considered essential in restoring the dentin's mechanical properties. More detailed data of the enzymes responsible and their detailed function in dentin-destructive conditions may not only help to find new and better preventive means, but better preservation of demineralized dentin collagenous matrix may also facilitate true biological remineralization for the better restoration of tooth structural and mechanical integrity and mechanical properties.
The regenerative endodontic procedure (REP) represents a treatment option for immature necrotic teeth with a periapical lesion. Currently, this therapy has a wide field of pre-clinical and clinical ...applications, but no standardization exists regarding successful criteria. Thus, by analysis of animal and human studies, the aim of this systematic review was to highlight the main characteristics of the tissue generated by REP. A customized search of PubMed, EMBASE, Scopus, and Web of Science databases from January 2000 to January 2022 was conducted. Seventy-five human and forty-nine animal studies were selected. In humans, the evaluation criteria were clinical 2D and 3D radiographic examinations. Most of the studies identified a successful REP with an asymptomatic tooth, apical lesion healing, and increased root thickness and length. In animals, histological and radiological criteria were considered. Newly formed tissues in the canals were fibrous, cementum, or bone-like tissues along the dentine walls depending on the area of the root. REP assured tooth development and viability. However, further studies are needed to identify procedures to successfully reproduce the physiological structure and function of the dentin–pulp complex.
Childhood is an ontogenetic stage unique to the modern human life history pattern. It enables the still dependent infants to achieve an extended rapid brain growth, slow somatic maturation, while ...benefitting from provisioning, transitional feeding, and protection from other group members. This tipping point in the evolution of human ontogeny likely emerged from early Homo. The GAR IVE hemi-mandible (1.8 Ma, Melka Kunture, Ethiopia) represents one of the rarely preserved early Homo infants (~ 3 years at death), recovered in a richly documented Oldowan archaeological context. Yet, based on the sole external inspection of its teeth, GAR IVE was diagnosed with a rare genetic disease-amelogenesis imperfecta (AI)-altering enamel. Since it may have impacted the child's survival, this diagnosis deserves deeper examination. Here, we reassess and refute this diagnosis and all associated interpretations, using an unprecedented multidisciplinary approach combining an in-depth analysis of GAR IVE (synchrotron imaging) and associated fauna. Some of the traits previously considered as diagnostic of AI can be better explained by normal growth or taphonomy, which calls for caution when diagnosing pathologies on fossils. We compare GAR IVE's dental development to other fossil hominins, and discuss the implications for the emergence of childhood in early Homo.
Bone is a hard-vascularized tissue, which renews itself continuously to adapt to the mechanical and metabolic demands of the body. The craniofacial area is prone to trauma and pathologies that often ...result in large bone damage, these leading to both aesthetic and functional complications for patients. The "gold standard" for treating these large defects is autologous bone grafting, which has some drawbacks including the requirement for a second surgical site with quantity of bone limitations, pain and other surgical complications. Indeed, tissue engineering combining a biomaterial with the appropriate cells and molecules of interest would allow a new therapeutic approach to treat large bone defects while avoiding complications associated with a second surgical site. This review first outlines the current knowledge of bone remodeling and the different signaling pathways involved seeking to improve our understanding of the roles of each to be able to stimulate or inhibit them. Secondly, it highlights the interesting characteristics of one growth factor in particular, FGF-2, and its role in bone homeostasis, before then analyzing its potential usefulness in craniofacial bone tissue engineering because of its proliferative, pro-angiogenic and pro-osteogenic effects depending on its spatial-temporal use, dose and mode of administration.
Introduction
Holmium:YAG(Ho:YAG) is currently the standard for lithotripsy. Superpulsed Thulium Fiber Laser(TFL) has been evaluated as an alternative for lithotripsy, using laser fibers with ...core-diameters(CDF) down to 50 µm and additional available settings suitable for “dusting” technique. This in-vitro study compared ablation rates, fissures and fragments’ size with 150µmCDF or 272µmCDF with different laser settings using TFL and Ho:YAG.
Methods
150CDF and 272CDF were compared using three settings for TFL “fine dusting”(FD:0.15 J/100 Hz); “dusting”(D:0.5 J/30 Hz); “fragmentation”(Fr:1 J/15 Hz) and Ho:YAG(D and Fr). An experimental setup consisting of immerged 10 mm cubes of artificial hard(H) or soft(S) stone phantoms was used with a 20 s’ lasing time and a spiral trajectory, in contact mode. Fragments (acquired through sieves) and stones were observed under optical microscopy before three-dimensional scanning to measure fragments and fissures(DOF) mean diameters and ablation volumes.
Results
Ablation volumes in with 150CDF-TFL and 272CDF-TFL were higher than those for 272CDF-Ho:YAG in both “dusting” (twofold and threefold) and “fragmentation”(1,5-fold and twofold). “Fine dusting” ablation rates with 150CDF-TFL and 272CDF-TFL were respectively at least 1,5-fold and twofold higher than those for 272CDF-Ho:YAG in “dusting”. 150CDF produced significantly smaller DOF than 272CDF in all settings against S and H except in fragmentation. 150CDF produced lower fragments’ diameter than 272CDF in all settings except dusting.
Conclusion
These preliminary studies demonstrate that at equal settings and CDF, TFL ablation rates are at least two-fold higher than those with Ho:YAG. 150CDF produces smaller fissures and fragments (that meets the definition of “dusting” lithotripsy) than 272CDF and higher ablation volumes than Ho:YAG.
The main goal of vital pulp therapy (VPT) is to preserve the vitality of the pulp tissue, even when it is exposed due to bacterial invasion, iatrogenic mechanical preparation, or trauma. The type of ...new dentin formed as a result of VPT can differ in its cellular origin, its microstructure, and its barrier function. It is generally agreed that the new dentin produced by odontoblasts (reactionary dentin) has a tubular structure, while the dentin produced by pulp cells (reparative dentin) does not or has less. Thus, even VPT aims to maintain the vitality of the pulp. It does not regenerate the dentin pulp complex integrity. Therefore, many studies have sought to identify new therapeutic strategies to successfully regenerate the dentin pulp complex. Among them is a Wnt protein-based strategy based on the fact that Wnt proteins seem to be powerful stem cell factors that allow control of the self-renewal and proliferation of multiple adult stem cell populations, suitable for homeostasis maintenance, tissue healing, and regeneration promotion. Thus, this review outlines the different agents targeting the Wnt signaling that could be applied in a tooth environment, and could be a potential therapy for dentin pulp complex and bone regeneration.
Introduction
Although thioredoxin-interacting protein (TXNIP) is involved in a variety of biological functions, the contribution of endothelial TXNIP has not been well-defined in regards to ...endothelial and vascular function or in post-ischemic revascularisation. We postulated that inhibition of endothelial TXNIP with siRNA or in a Cre-LoxP system could be involved in protection from high fat, high protein, low carbohydrate (HFHPLC) diet-induced oxidative stress and endothelial dysfunction, leading to vascular damage and impaired revascularisation in vivo.
Methods and results
To investigate the role of endothelial TXNIP, the TXNIP gene was deleted in endothelial cells using anti-TXNIP siRNA treatment or the Cre-LoxP system. Murine models were fed a HFHPLC diet, known to induce metabolic disorders. Endothelial TXNIP targeting resulted in protection against metabolic disorder-related endothelial oxidative stress and endothelial dysfunction. This protective effect mitigates media cell loss induced by metabolic disorders and hampered metabolic disorder-related vascular dysfunction assessed by aortic reactivity and distensibility. In aortic ring cultures, metabolic disorders impaired vessel sprouting and this alteration was alleviated by deletion of endothelial TXNIP. When subjected to ischemia, mice fed a HFHPLC diet exhibited defective post-ischemic angiogenesis and impaired blood flow recovery in hind limb ischemia. However, reducing endothelial TXNIP rescued metabolic disorder-related impairment of ischemia-induced revascularisation.
Conclusion
Collectively, these results show that targeting endothelial TXNIP in metabolic disorders is essential to maintaining endothelial function, vascular function and improving ischemia-induced revascularisation, making TXNIP a potential therapeutic target for therapy of vascular complications related to metabolic disorders.
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