ABSTRACT
tem cells have an inherent capacity to facilitate regeneration; this has led to unprecedented growth in their experimental use in various clinical settings, particularly in patients with diseases with few alternative treatment options. However, their approved clinical use has to date been restricted largely to haematological diseases and epidermal transplantation to treat severe burns. After thorough searching of two databases, this review illuminates the role of stem cell therapy for treatment of musculoskeletal diseases. Research suggests that successful application of stem cells as regenerative mediators is in all likelihood dependent on the ability of endogenous tissue-resident reparative mediators to respond to paracrine signals provided by the applied stem cells. Therefore, an understanding of how the pathological environment influences this process is crucial for the ultimate success of stem cell therapies. The current review presents both the progress and limitations of stem cells as regenerative mediators in the context of musculoskeletal disorders
Subject(s)
Cells , Musculoskeletal Physiological Phenomena , Regenerative Medicine , South AfricaABSTRACT
Background: Sickle cell anemia (SCA) forms one of the neglected tropical disease of genetic aetiology. Unlike many complex genetic diseases inherited on a multiallelic pattern; SCA is a hemoglobinopathy of Mendelian type genetic inheritance. The SCA trait is inherited through a recessive autosomal link; with the homozygotes(SS) manifesting clinical disease; while the heterozygoste(AS) are clinically normal-exept in states of hypoxia or severe infection. Method: Review of relevant literature on bone marrow transplantation and gene replacement therapy in sickle cell anaemia was obtained from texts and Pubmed search. Results: The exact genetic disorder assailing SCA is the production of mutant or abnormal a peptide chains in which the amino acid Glutamine has been substituted with valine. The issuing Haemoglobin polymerizes when deoxygenated;causing constituent RBCs to sickle; haemolyse and block small blood vessels- a clinical state that manifests as haemolytic anemia; aplasia; thrombo-embolic phenomenon; or painful crises. Unfortunately; up to day; there is no cure to SCA; and management only aims at preventing or ameliorating attacks. Conclusion: By virtue of its well defined and localized genetic aetiopathophysiology; and the advances in gene replacement therapy and regenerative medicine; we argue here the case for Bone marrow transplantation (BMT) and Gene replacement therapy (GRT) in sickle cell anemia
Subject(s)
Anemia , Bone Marrow Transplantation , Regenerative MedicineABSTRACT
Background: Sickle cell anemia (SCA) forms one of the neglected tropical disease of genetic aetiology. Unlike many complex genetic diseases inherited on a multiallelic pattern; SCA is a hemoglobinopathy of Mendelian type genetic inheritance. The SCA trait is inherited through a recessive autosomal link; with the homozygotes(SS) manifesting clinical disease; while the heterozygoste(AS) are clinically normal-exept in states of hypoxia or severe infection. Method: Review of relevant literature on bone marrow transplantation and gene replacement therapy in sickle cell anaemia was obtained from texts and Pubmed search. Results: The exact genetic disorder assailing SCA is the production of mutant or abnormal a peptide chains in which the amino acid Glutamine has been substituted with valine. The issuing Haemoglobin polymerizes when deoxygenated;causing constituent RBCs to sickle; haemolyse and block small blood vessels- a clinical state that manifests as haemolytic anemia; aplasia; thrombo-embolic phenomenon; or painful crises. Unfortunately; up to day; there is no cure to SCA; and management only aims at preventing or ameliorating attacks. Conclusion: By virtue of its well defined and localized genetic aetiopathophysiology; and the advances in gene replacement therapy and regenerative medicine; we argue here the case for Bone marrow transplantation (BMT) and Gene replacement therapy (GRT) in sickle cell anemia