Non-pharmacological treatment of osteoporosis with Nuclear Magnetic Resonance Therapy (NMR-Therapy)

Objectives: To demonstrate the long-term effects of the therapeutic use of nuclear magnetic resonance (NMR) on bone mineral density (BMD) parameters in patients with osteoporosis. Methods: We enrolled 103 patients aged between 45 and 89 years who had osteoporosis with a T-score of bone mineral density less than -2.5. All patients received an osteoporosis treatment with low field nuclear magnetic resonance using a special NMR device (MBST, MedTec, Germany) for one hour per day on 10 consecutive days. At baseline and 12 months after NMR treatment the BMD was measured by DEXA. Additionally, the levels of the bone turnover markers osteocalcin and bone crosslaps (B-CTX; crosslinked telopeptides of collagen 1) were measured by immunoassays. Results: BMD and serum levels of osteocalcin increased significantly from baseline to 12 months. B-CTX remained stable. Conclusions: Under therapeutically use of NMR-Therapy, BMD-parameters increased during 12 months after a treatment block (10 x 1h). Therefore, NMR-Therapy can be considered a useful alternative or supplement to medical therapy in patients with osteoporosis

Rehabilitation of knee osteoarthritis - comparison study: Nuclear magnetic resonance therapy (MBST) versus conventional physiotherapy”.

CILJ: Usporediti učinkovitost terapijske nuklearne magnetske rezonance niske energije (MBST® terapije) u odnosu na fizioterapiju u liječenju bolesnika sosteoartritisom koljena prateći parametre: bol, pokretljivost, snagu ifunkcionalnu sposobnost bolesnika. METODE:32 bolesnika s dijagnozom osteoartritisa koljena bilo je podijeljeno u tri skupine prema vrsti terapije koju su provodili: u skupinikoja je provodila fizioterapijubilo je 10 ispitanika (FT10), u skupini koja je provodila MBST® terapiju za oba koljena 14 ispitanika (MBST7) i u skupini koja je provodila MBST® terapiju za jedno koljeno8 ispitanika (MBST9).Inicijalno mjerenje i procjena provođeni su prvi dan terapije te su mjerenja ponovljena zadnji dan terapije. Kontrolna mjerenja provođena su mjesec dana nakon obavljene terapije te završno mjerenje i procjena tri mjeseca nakon obavljene terapije. Metode procjene koje su primijenjene su Lequesne upitnik za procjenu funkcionalne sposobnosti, Numerička skala boli (NRS), mjerenje mišićne snage ekstenzora koljena pomoću mehaničke vage i mjerenje opsega pokreta u koljenu goniometrom. REZULTATI: U analizi utjecaja vrste terapijena opseg pokreta koljena, na mišićnu snagu ekstenzora koljena te na razinu boli po mjerenjima nije bilo statistički značajne razlike između ispitivanih skupina. U analizi utjecaja vrste terapijena funkcionalnu sposobnost, utvrđene su statistički značajne razlike između skupina MBST7i FT10te skupina MBST9i FT10,u korist MBST® metode.OBJECTIVES: To determine the efficiency of the magnetic resonance therapy (MBST®) in comparison to the traditional physiotherapy approach in treatment of patients with osteoarthritis of the knee joint using the following parameters: pain, mobility, strength and functional ability. METHODS: 32 patients with diagnosed osteoarthritis of the knee were divided into three groups with respect to the therapyapplied: 10 in the physiotherapy group (FT10), 14 in the MBST for both knees group (MBST7) and 8 in the MBST for one knee group (MBST9). Initial measurements and evaluation had been conducted on the first day of the therapyand measurements were then repeated on the last day of the therapy, as well as one month after the therapy.Three months after the therapy final measurements and evaluation were done. Methods used for the evaluation were:Lequesne questionnaire for the assessment of functional abilities, the numeric pain rating scale (NRS), measuring the knee extensor muscle strength using mechanical balance and assessment of the knee’s range of motion using the goniometer. RESULTS: There was no statistically significant difference observed forthe knee’s range of motion, kneeextensor muscle strength orthe level of pain between tested groups. The statistically significant difference was present for the functional ability, where bothMBST7 and MBST9 showed better results than FT10 therapy

Clinical Parameters in Osteoporosis Patients Supplemented With PMA-Zeolite at the End of 5-Year Double-Blinded Clinical Trial

Osteoporosis is among the most common pathologies. Associated complications in osteoporotic patients, in particular hip fractures and vertebral fractures, cause disabilities and significant quality of life deterioration. Standard treatment of osteoporosis, based on pharmacotherapy does still not yield adequate results, and the problem of osteoporosis remains incompletely solved. Additionally, adverse drug events and fractures after longtermed pharmacotherapy pose additional challenges within designing a proper therapy regimen. Improved clinical approach and new synergistic treatment modalities are consequently still needed. The rationale of the presented study was accordingly, to expand our preclinical animal study on human patients with osteoporosis, based on positive effects on bones observed in animals with osteopenia treated with PMA-zeolite. We specifically monitored effects of PMA-zeolite on the bone quality parameters, fracture risk and quality of life in a cohort of initially recruited 100 osteoporosis patients during a follow-up period of 5 years within a randomized, placebo-controlled and double blinded clinical study (TOP study). Obtained results provide evidence on the PMA-zeolite positive effects on the bone strength of osteoporotic patients as the risk of fractures was significantly decreased in PMA-zeolite-treated patients with respect to time before entering the study (p = 0.002). Statistical evidence point also to positive bone changes in the 5-years TOP study course as evidenced through osteocalcin and beta-cross laps values showing a prevalence of the bone-formation process (p < 0.05). BMD values were not significantly affected after the 5-years follow-up in PMA-zeolite-treated patients in comparison with the Placebo group. Results support the initial expectations based on our previously published preclinical studies on clinoptilolite product PMA-zeolite in animals that could be a new therapeutic option in osteoporosis patients

X-Linked Osteogenesis Imperfecta Possibly Caused by a Novel Variant in PLS3

Osteogenesis imperfecta (OI) represents a complex spectrum of genetic bone diseases that occur primarily due to mutations and deletions of the COL1A1 and COL1A2 genes. Recent molecular studies of the network of signaling pathways have contributed to a better understanding of bone remodeling and the pathogenesis of OI caused by mutations in many other genes associated with normal bone mineralization. In this paper, a case of a rare X-linked variant of OI with a change in the gene encoding plastin 3&mdash;a protein important for the regulation of the actin cytoskeleton, is presented. A 16-year-old patient developed ten bone fractures caused by minor trauma or injury, including a compression fracture of the second lumbar vertebra during his lifetime. Next-generation sequencing analysis did not show pathologically relevant deviations in the COL1A1 and COL1A2 genes. Targeted gene analyses (Skeletal disorder panel) of the patient, his father, mother and sister were then performed, detecting variants of uncertain significance (VUS) for genes PLS3, FN1 and COL11A2. A variant in the PLS3 gene were identified in the patient, his mother and sister. Since the PLS3 gene is located on the X chromosome, the mother and sister showed no signs of the disease. Although the variant in the PLS3 gene (c.685G&gt;A (p.Gly229Arg)) has not yet been described in the literature, nor is its pathogenicity known, clinical findings combined with genetic testing showed that this variant may explain the cause of X-linked OI in our patient. This rare case of the PLS3 variant of X-linked OI might point to a novel target for personalized therapy in patients with this severe disease

X-Linked Osteogenesis Imperfecta Possibly Caused by a Novel Variant in PLS3

Osteogenesis imperfecta (OI) represents a complex spectrum of genetic bone diseases that occur primarily due to mutations and deletions of the COL1A1 and COL1A2 genes. Recent molecular studies of the network of signaling pathways have contributed to a better understanding of bone remodeling and the pathogenesis of OI caused by mutations in many other genes associated with normal bone mineralization. In this paper, a case of a rare X-linked variant of OI with a change in the gene encoding plastin 3—a protein important for the regulation of the actin cytoskeleton, is presented. A 16-year-old patient developed ten bone fractures caused by minor trauma or injury, including a compression fracture of the second lumbar vertebra during his lifetime. Next- generation sequencing analysis did not show pathologically relevant deviations in the COL1A1 and COL1A2 genes. Targeted gene analyses (Skeletal disorder panel) of the patient, his father, mother and sister were then performed, detecting variants of uncertain significance (VUS) for genes PLS3, FN1 and COL11A2. A variant in the PLS3 gene were identified in the patient, his mother and sister. Since the PLS3 gene is located on the X chromosome, the mother and sister showed no signs of the disease. Although the variant in the PLS3 gene (c.685G>A (p.Gly229Arg)) has not yet been described in the literature, nor is its pathogenicity known, clinical findings combined with genetic testing showed that this variant may explain the cause of X-linked OI in our patient. This rare case of the PLS3 variant of X-linked OI might point to a novel target for personalized therapy in patients with this severe disease

X-Linked Osteogenesis Imperfecta Possibly Caused by a Novel Variant in PLS3

Osteogenesis imperfecta (OI) represents a complex spectrum of genetic bone diseases that occur primarily due to mutations and deletions of the COL1A1 and COL1A2 genes. Recent molecular studies of the network of signaling pathways have contributed to a better understanding of bone remodeling and the pathogenesis of OI caused by mutations in many other genes associated with normal bone mineralization. In this paper, a case of a rare X-linked variant of OI with a change in the gene encoding plastin 3—a protein important for the regulation of the actin cytoskeleton, is presented. A 16-year-old patient developed ten bone fractures caused by minor trauma or injury, including a compression fracture of the second lumbar vertebra during his lifetime. Next- generation sequencing analysis did not show pathologically relevant deviations in the COL1A1 and COL1A2 genes. Targeted gene analyses (Skeletal disorder panel) of the patient, his father, mother and sister were then performed, detecting variants of uncertain significance (VUS) for genes PLS3, FN1 and COL11A2. A variant in the PLS3 gene were identified in the patient, his mother and sister. Since the PLS3 gene is located on the X chromosome, the mother and sister showed no signs of the disease. Although the variant in the PLS3 gene (c.685G>A (p.Gly229Arg)) has not yet been described in the literature, nor is its pathogenicity known, clinical findings combined with genetic testing showed that this variant may explain the cause of X-linked OI in our patient. This rare case of the PLS3 variant of X-linked OI might point to a novel target for personalized therapy in patients with this severe disease