Abstract
Osteoarthritis (OA) is one of the main causes of morbidity in the world population, being one of the main factors of occupational incapacity in countries like United States and Brazil. Chronic pain associated with OA is the main phenomenon that translates the incapacitation in the individuals affected, generating a direct impact on their quality of life. OA pain therapy is limited and unsatisfactory, made by the use of corticosteroids and anti-inflammatories, which in chronic use, harm patients' clinical status, offering few benefits. In this sense, the use of regenerative therapies such as Platelet-Rich Plasma (PRP) has been highlighted because of its greater effectiveness in the treatment of OA. The presence of several growth factors in the platelets, released through its activation, increase the tissue regeneration of the patients, providing a better prognosis compared to other therapies used in OA treatment. However, despite the promising character, there is a lack of data regarding the molecular mechanisms by which PRP exhibits its action for tissue regeneration and analgesia of the joint compartment, especially in the cartilaginous tissue, one of the main targets of Osteoarthritis. Previously in-vitro studies have shown that peripherally, Brain-Derived Neurotrophic Factor (BDNF) acts on chondrocyte differentiation, aiding in the synthesis of cartilaginous tissue, and furthermore, contributes to macrophage modulation for anti-inflammatory phenotype. Thus, the present work aims to investigate the molecular mechanisms involved in the pharmacological action of BDNF, a neurotrophic growth factor present in platelets, during PRP therapy, in experimental Osteoarthritis model. (AU)
|