RESUMO
Thyroid hormones are important factors that regulate metabolism and cell differentiation throughout the human body. A complication of thyroid pathology is represented by an alteration of the bone metabolism which can lead to osteoporosis and fragility fractures, known to have a high mortality rate. Although there is a consensus on the negative impact of hyperthyroidism on bone metabolism, when referring to hypothyroidism, subclinical hypothyroidism, or subclinical hyperthyroidism, there is no general agreement. The aim of our review was to update clinicians and researchers about the current data regarding the bone health in hypothyroidism, subclinical hypothyroidism, and subclinical hyperthyroidism patients. Thyroid disorders have an important impact on bone metabolism and fracture risk, such that hyperthyroidism, hypothyroidism, and subclinical hyperthyroidism are associated with a decreased bone mineral density (BMD) and increased risk of fracture. Subclinical hypothyroidism, on the other hand, is not associated with osteoporosis or fragility fractures, and subclinical hyperthyroidism treatment with radioiodine could improve bone health.
RESUMO
Articular cartilage has a complex structure and metabolism which allow for a proper movement within joints. Nevertheless, several systemically administered pharmacological agents have been proved to improve the anabolic response in the case of cartilage lesions. Alendronate, glucosamine, chondroitin sulfate, hyaluronic acid, collagen hydrolysate, vitamin C, vitamin D, aspirin and strontium ranelate have shown positive results in clinical trials. On the other hand, calcitonin, risedronate, doxycycline, and celecoxib did not slow the progression of cartilage lesions in clinical trials. Other systemic drugs or supplements such as teriparatide, leptin, zoledronic acid, bevacizumab, atorvastatin, omega-3 fatty acid, naringin, MSM, selenium, zinc, magnesium, resveratrol, donepezil, naproxen, etodolac, ursodeoxycholic acid (UDCA), lithium chloride, and rebamipide showed positive results in in vitro and animal studies but clinical trials are needed to confirm the positive impact on cartilage repair. A number of molecules, not currently available on the market, have also shown promising results in cartilage healing, such as licofelone, sclerostin, cyclopamine, cyclodextrin polysulfate, AG-041R, osteoprotegerin, rhMK, ß-cryptoxanthine, NF-κb essential modulator binding domain (NBD), TGF-ß-neutralizing antibody, osteogenic protein-1 (BMP-7), fibroblast growth factor 2 (FGF2), and RhBMP-2. Currently available systemic drugs that impair cartilage healing are represented by corticosteroids, vitamin A, and fluoroquinolones.
