Osteoporosis and cardiovascular diseases are common causes of morbidity and mortality worldwide, especially in people aged over 60 years. Osteoporosis is characterized by low bone mineral density, which deteriorates the microarchitecture of bones and increases the risk of bone fractures. Other pathologies also constitute risk factors for the development of osteoporosis, mainly cardiovascular diseases. In fact, a growing number of reports have shown a positive correlation between cardiovascular diseases and low bone mineral density. MMPs are proteases that participate in the organized degradation of the extracellular matrix (ECM) and which play essential physiological roles, such as cardiovascular and bone tissue remodeling. Overexpression of MMPs underlies pathological processes like osteoporosis and cardiovascular diseases. MMP-1, -2, -9, -13, and -14 are expressed in bone tissue and are key players in the digestion of bone matrix by osteoblasts. Considering this relationship between osteometabolic and cardiovascular pathologies and MMPs, this review focuses on the involvement of MMPs in osteoporosis and on their participation in cardiovascular diseases; it also deals with the positive correlation between osteoporosis and cardiovascular diseases. Although there are many drugs to treat osteoporosis, controversies exist. Here, we will describe these controversies and will discuss how inhibition of MMPs could be an alternative strategy to or an adjuvant therapy in the current treatment of osteoporosis.

Bone grafts are used in the medical-surgical field for anatomical and functional reconstruction of lost bone areas, aiding the bone repair process by osteogenesis, osteinduction and osteoconduction. New materials such as F1 (fraction 1) protein extracted from the rubber tree Hevea brasiliensis have been investigated and currently present important properties for tissue repair, and are associated with neoangiogenesis, promoting cell adhesion and extracellular matrix formation. The main objective of this study was to investigate the association of F1 protein to different bone grafts in the repair of critical bone defects in the calvaria of Wistar rats. A total of 112 Wistar rats were divided as follows: autograft (AuG), allograft (AlG), xenograft (XeG), autograft/F1 (AuG–F1), allograft/F1 (AlG–F1), xenograft/F1 (XeG–F1), F1 (F1), control (CTL), with a waiting period of 4 and 6 weeks (w). The stereological AuG, AlG, AuG–F1 and AlG–F1 results had greater bone neoformation ( p < 0.05). For immunohistochemistry, the angiogenic and osteogenic factors were higher for AuG–F1 and AlG–F1. TRAP-positive cells were higher in XeG–F1 and AlG (37 ± 9.53, 13.3 ± 4.16) (4 w) and XeG, AlG–F1 and XeG–F1 (20.33 ± 7.37; 15.25 ± 6.02, 19.33 ± 3.21) (6 w). For zymography, F1 showed increased gelatinolytic activity of MMP-2 and -9. It was concluded that the bone graft associated or not with F1 increases the angiogenic and osteogenic, biochemical and stereological factors.

The aim of this research was to evaluate the fracture healing area in osteoporotic femur of female rats restrained by stainless steel wire by statin administration in two different doses (5 mg and 20 mg). Ninety female rats were divided into six groups (n = 15): SH, SH-5 mg, SH-20 mg, OVX, OVX-5 mg, and OVX-20 mg. The surgery consisted of the fracture of the left femur bone and stabilization by K-wire and the administration was restricted and weekly controlled in the drinking water. The euthanasia was conducted at three different moments, five animals per period: 7 d, 14 d, and 28 d. Densitometry, zymography, and histological analyses showed a significant difference between some groups. According to these findings, simvastatin promoted a positive action for bone repair, especially in the osteometabolic group treated with 20 mg of the drug.