Oral Health in Patients with History of Head and Neck Cancer: Complexity and Benefits of a Targeted Oral Healthcare Pathway.

PURPOSE OF REVIEW: This work consists in a literature review on the current state of knowledge regarding the oral management of patients with a history of head and neck cancer (HNC), corroborated by clinical cases and illustrated by clear infographic summaries. It aims to provide healthcare professionals with a comprehensive overview of the oral health status of HCN patients. RECENT FINDINGS: Head and neck cancers (HNCs) represent the seventh most common type of cancer worldwide, with over 660,000 annual new cases. Despite the significant negative impact of HNCs on oral health, patients often receive no or inappropriate oral care while the significant impact of oral pathologies on cancer prognosis is commonly underestimated. This work (i) describes the oral cavity during and after HNC through the prism of care complexity and (ii) highlights several potential key factors that could worsen long-time patients' prognosis and quality of life. By investigating the biological, microbiological, functional, and psychological dimensions of the interrelationships between HNCs and oral health, the authors explored the barriers and benefits of a targeted oral healthcare pathway. This article emphasizes the importance of multidisciplinary care and highlights the need for further research elucidating the intricate relationships between oral health and HNCs, particularly through the microbiota.

Unprepared areas and centralization of oval canals prepared with WaveOne Gold or XP-endo Shaper: microcomputed tomographic analyses / Areas não preparadas e centralização de canais ovais preparados com WaveOne Gold ou XP-endo Shaper: análises tomográficas microcomputadorizadas

ABSTRACT Current instrumentation systems cannot fully prepare oval root canal systems. This may cause accumulation of hard tissue debris and fail to eliminate bacteria from areas inaccessible to instrumentation, which could perpetuate periapical inflammation and jeopardize the success of endodontic treatment Aim To evaluate the performance of two endodontic systems in oval canals by investigating the changes in volume, unprepared areas, and centering ability of XP-endo Shaper (XPS) and WaveOne Gold (WOG) in oval canals using microcomputed tomography (micro-CT) Materials and Method Thirty mandibular canines were scanned before and after preparation with WOG (25/.07 and 35/.06) or XPS (30/.01) to evaluate the volume, surface area, and canal centralization at 4 mm and 10 mm from the apical foramen Results Volume and surface area increased significantly after preparation with both systems (p<0.05). However, no significant difference was observed in the unprepared areas, regarding either the entire canal (26.21% for WOG and 30.10% for XPS), or the apical segment (18.82% for WOG and 14.63% for XPS) (p >0.05) Conclusions Both systems maintained canal centralization, with no difference between them. XPS and WOG had similar shaping abilities in the mandibular canine, but left almost one third of the unprepared areas.

RESUMO Os sistemas de instrumentação atuais são incapazes de preparar completamente os sistemas de canais radiculares do canal oval, o que pode levar ao acúmulo de detritos de tecido duro e manter micro-organismos em áreas inacessíveis à instrumentação. Essas bactérias poderiam perpetuar a inflamação periapical e comprometer o sucesso do tratamento endodôntico Objetivo Para avaliar o comportamento de dois sistemas endodônticos em canais ovais, esse estudo investigou as alterações no volume, áreas não preparadas e capacidade de centralização do XP-endo Shaper (XPS) e do WaveOne Gold (WOG) em canais ovais usando microtomografia computadorizada (micro-CT) Material e métodos Trinta caninos inferiores foram escaneados antes e depois do preparo com WOG (25/.07 e 35/.06) ou XPS (30/.01) para avaliar o volume, a área de superfície e a centralização do canal a 4 mm e 10 mm do forame apical Resultados O volume e a área de superfície aumentaram significativamente após o preparo com ambos os sistemas (p<0,05). No entanto, não foram observadas diferenças significativas nas áreas não preparadas, não apenas em todo o canal (26,21% para WOG e 30,10% para XPS), mas também no segmento apical (18,82% para WOG e 14,63% para XPS) (p >0,05) Conclusão Ambos os sistemas mantiveram a centralização do canal, sem diferenças entre eles. O XPS e o WOG tiveram habilidades de modelagem semelhantes no canino mandibular, mas deixaram quase um terço das áreas do canal sem preparo.

Genetic Ablation of Osteopontin in Osteomalacic Hyp Mice Partially Rescues the Deficient Mineralization Without Correcting Hypophosphatemia.

PHEX is predominantly expressed by bone and tooth-forming cells, and its inactivating mutations in X-linked hypophosphatemia (XLH) lead to renal phosphate wasting and severe hypomineralization of bones and teeth. Also present in XLH are hallmark hypomineralized periosteocytic lesions (POLs, halos) that persist despite stable correction of serum phosphate (Pi ) that improves bulk bone mineralization. In XLH, mineralization-inhibiting osteopontin (OPN, a substrate for PHEX) accumulates in the extracellular matrix of bone. To investigate how OPN functions in Hyp mice (a model for XLH), double-null (Hyp;Opn-/- ) mice were generated. Undecalcified histomorphometry performed on lumbar vertebrae revealed that Hyp;Opn-/- mice had significantly reduced osteoid area/bone area (OV/BV) and osteoid thickness of trabecular bone as compared to Hyp mice, despite being as hypophosphatemic as Hyp littermate controls. However, tibias examined by synchrotron radiation micro-CT showed that mineral lacunar volumes remained abnormally enlarged in these double-null mice. When Hyp;Opn-/- mice were fed a high-Pi diet, serum Pi concentration increased, and OV/BV and osteoid thickness normalized, yet mineral lacunar area remained abnormally enlarged. Enpp1 and Ankh gene expression were increased in double-null mice fed a high-Pi diet, potentially indicating a role for elevated inhibitory pyrophosphate (PPi ) in the absence of OPN. To further investigate the persistence of POLs in Hyp mice despite stable correction of serum Pi , immunohistochemistry for OPN on Hyp mice fed a high-Pi diet showed elevated OPN in the osteocyte pericellular lacunar matrix as compared to Hyp mice fed a control diet. This suggests that POLs persisting in Hyp mice despite correction of serum Pi may be attributable to the well-known upregulation of mineralization-inhibiting OPN by Pi , and its accumulation in the osteocyte pericellular matrix. This study shows that OPN contributes to osteomalacia in Hyp mice, and that genetic ablation of OPN in Hyp mice improves the mineralization phenotype independent of systemic Pi -regulating factors. © 2020 American Society for Bone and Mineral Research.

Osteopontin and the dento-osseous pathobiology of X-linked hypophosphatemia.

Seven young patients with X-linked hypophosphatemia (XLH, having inactivating PHEX mutations) were discovered to accumulate osteopontin (OPN) at the sites of defective bone mineralization near osteocytes - the so-called hallmark periosteocytic (lacunar) "halos" of XLH. OPN was also localized in the pericanalicular matrix extending beyond the osteocyte lacunae, as well as in the hypomineralized matrix of tooth dentin. OPN, a potent inhibitor of mineralization normally degraded by PHEX, is a member of a family of acidic, phosphorylated, calcium-binding, extracellular matrix proteins known to regulate dental, skeletal, and pathologic mineralization. Associated with the increased amount of OPN (along with inhibitory OPN peptide fragments) in XLH bone matrix, we found an enlarged, hypomineralized, lacuno-canalicular network - a defective pattern of skeletal mineralization that decreases stiffness locally at: i) the cell-matrix interface in the pericellular environment of the mechanosensing osteocyte, and ii) the osteocyte's dendritic network of cell processes extending throughout the bone. Our findings of an excess of inhibitory OPN near osteocytes and their cell processes, and in dentin, spatially correlates with the defective mineralization observed at these sites in the skeleton and teeth of XLH patients. These changes likely contribute to the dento-osseous pathobiology of XLH, and participate in the aberrant bone adaptation and remodeling seen in XLH.

Abnormal presence of the matrix extracellular phosphoglycoprotein-derived acidic serine- and aspartate-rich motif peptide in human hypophosphatemic dentin.

Severe dental troubles are associated with X-linked hypophosphatemic rickets and are mainly related to impaired dentin mineralization. In dentin matrix, matrix extracellular phosphoglycoprotein (MEPE) may be protected from proteolysis by a specific interaction with PHEX (phosphate regulating gene with homologies to endopeptidases on the X chromosome). The objective of our work was to determine whether PHEX impairment induces MEPE cleavage in dentin and the subsequent release of the C-terminal acidic serine- and aspartate-rich motif (ASARM) peptide, which is known to inhibit mineralization. By Western blot analysis, we explored dentin extracts from seven hypophosphatemic patients with mutations of the PHEX gene. A proteomic approach combining immunoprecipitation, surface-enhanced laser desorption/ionization-time of flight-mass spectrometry and matrix-assisted laser desorption ionization-time of flight analysis of the samples completed this exploration. This study shows a 4.1-kDa peptide containing the MEPE-derived ASARM peptide in hypophosphatemic samples. The presence of ASARM was less marked in patients treated with 1-hydroxylated vitamin D and phosphate during growth. Moreover, recombinant ASARM implanted in a rat pulp injury model disturbed the formation of the reparative dentin bridge. These results suggest that abnormal MEPE cleavage occurs when PHEX activity is deficient in humans, the ASARM peptide may be involved in the mineralization defects and the PHEX-MEPE interaction may be indirect, as ensuring a better phosphate and vitamin D environment to the mineralizing dentin prevents MEPE cleavage.