Browsing by Subject "rickets"

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  • Österlund, Michaela (Helsingfors universitet, 2017)
    Detta arbete är en litteraturstudie vars syfte är att undersöka vetenskapliga artiklar för att ta reda på hur D-vitamin påverkar parodontala vävnaden och om det finns belägg för att D-vitamin har en positiv effekt på parodontala hälsan. D-vitamin är ett prohormon som reglerar immunförsvaret och kroppens absorption av kalcium och fosfor. Parodontit är en kronisk inflammatorisk sjukdom som bryter ner tänders stödjevävnad samt käkarnas alveolarben och ger upphov till tandlossning. Denna studie letar i den vetenskapliga litteraturen om det finns kausalitets samband mellan D-vitaminbrist och parodontit eftersom båda tillstånden är skelettala och inflammatoriska sjukdomar. Både parodontit och D-vitaminbrist är vanligt förekommande i den finska befolkningen. Detta arbete är baserat på litteratursökning i PubMed, Melinda, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews och internet hemsidan terveysportti.fi. Litteraturgranskningens resultat är att sambandet mellan D-vitamin halten i serum och parodontal infektion är svag. Populations studier visar att D-vitamin brist har försumbar gynnsam effekt på parodontal infektion. Däremot har D-vitamin i teorin positiv effekt på alveolarbenets mineraldensitet och immunförsvar. Denna studie visar att D-vitaminbrist kan vara orsaken till ett svagt parodontologiskt behandlingssvar om andra starkare parodontologiska riskfaktorer är uteslutna.
  • Beck-Nielsen, Signe Sparre; Mughal, Zulf; Haffner, Dieter; Nilsson, Ola; Levtchenko, Elena; Ariceta, Gema; Collantes, Carmen de Lucas; Schnabel, Dirk; Jandhyala, Ravi; Mäkitie, Outi (2019)
    Background: X-linked hypophosphatemia (XLH) is an inherited disease of phosphate metabolism in which inactivating mutations of the Phosphate Regulating Endopeptidase Homolog, X-Linked (PHEX) gene lead to local and systemic effects including impaired growth, rickets, osteomalacia, bone abnormalities, bone pain, spontaneous dental abscesses, hearing difficulties, enthesopathy, osteoarthritis, and muscular dysfunction. Patients with XLH present with elevated levels of fibroblast growth factor 23 (FGF23), which is thought to mediate many of the aforementioned manifestations of the disease. Elevated FGF23 has also been observed in many other diseases of hypophosphatemia, and a range of animal models have been developed to study these diseases, yet the role of FGF23 in the pathophysiology of XLH is incompletely understood. Methods: The role of FGF23 in the pathophysiology of XLH is here reviewed by describing what is known about phenotypes associated with various PHEX mutations, animal models of XLH, and non-nutritional diseases of hypophosphatemia, and by presenting molecular pathways that have been proposed to contribute to manifestations of XLH. Results: The pathophysiology of XLH is complex, involving a range of molecular pathways that variously contribute to different manifestations of the disease. Hypophosphatemia due to elevated FGF23 is the most obvious contributor, however localised fluctuations in tissue non-specific alkaline phosphatase (TNAP), pyrophosphate, calcitriol and direct effects of FGF23 have been observed to be associated with certain manifestations. Conclusions: By describing what is known about these pathways, this review highlights key areas for future research that would contribute to the understanding and clinical treatment of non-nutritional diseases of hypophosphatemia, particularly XLH.
  • Beck-Nielsen, Signe S; Mughal, Zulf; Haffner, Dieter; Nilsson, Ola; Levtchenko, Elena; Ariceta, Gema; de Lucas Collantes, Carmen; Schnabel, Dirk; Jandhyala, Ravi; Mäkitie, Outi (BioMed Central, 2019)
    Abstract Background X-linked hypophosphatemia (XLH) is an inherited disease of phosphate metabolism in which inactivating mutations of the Phosphate Regulating Endopeptidase Homolog, X-Linked (PHEX) gene lead to local and systemic effects including impaired growth, rickets, osteomalacia, bone abnormalities, bone pain, spontaneous dental abscesses, hearing difficulties, enthesopathy, osteoarthritis, and muscular dysfunction. Patients with XLH present with elevated levels of fibroblast growth factor 23 (FGF23), which is thought to mediate many of the aforementioned manifestations of the disease. Elevated FGF23 has also been observed in many other diseases of hypophosphatemia, and a range of animal models have been developed to study these diseases, yet the role of FGF23 in the pathophysiology of XLH is incompletely understood. Methods The role of FGF23 in the pathophysiology of XLH is here reviewed by describing what is known about phenotypes associated with various PHEX mutations, animal models of XLH, and non-nutritional diseases of hypophosphatemia, and by presenting molecular pathways that have been proposed to contribute to manifestations of XLH. Results The pathophysiology of XLH is complex, involving a range of molecular pathways that variously contribute to different manifestations of the disease. Hypophosphatemia due to elevated FGF23 is the most obvious contributor, however localised fluctuations in tissue non-specific alkaline phosphatase (TNAP), pyrophosphate, calcitriol and direct effects of FGF23 have been observed to be associated with certain manifestations. Conclusions By describing what is known about these pathways, this review highlights key areas for future research that would contribute to the understanding and clinical treatment of non-nutritional diseases of hypophosphatemia, particularly XLH.