Cigarette smoking has a negative impact on the skeletal system by reducing bone mass and increasing the risk of fractures through its direct or indirect effects on bone remodeling. Recent evidence shows that smoking causes an imbalance in bone turnover, making bone vulnerable to osteoporosis and fragility fractures. In addition, cigarette smoking is known to have deleterious effects on fracture healing, as a positive correlation has been shown between the daily number of cigarettes smoked and years of exposure to smoking, although the underlying mechanisms are not fully understood. Smoking is also known to cause several medical and surgical complications responsible for longer hospital stays and a consequent increase in resource consumption. Smoking cessation is, therefore, highly advisable to prevent the onset of metabolic bone disease. However, some of the consequences appear to continue for decades. Based on this evidence, the aim of our work was to assess the impact of smoking on the skeletal system, particularly bone fractures, and to identify the pathophysiological mechanisms responsible for the impairment of fracture healing. Because smoking represents a major public health problem, understanding the association between cigarette smoking and the occurrence of bone disease is necessary in order to identify potential new targets for intervention.
The study describes the changes of condrocytes and extracellular matrix occurring in Hip OA. 16 femoral heads were included in the study. Cartilage explants were removed from 3 anatomical sites over the surface of 14 OA and 2 non-OA patients. Cartilage sections were evaluated with histological (EE, Alcian Blu and Mallory-Azan stainings) and immuno-histochemichal (antibodies directed against fibronectin, tenascin, laminin, type I and type IV collagen, metallo-proteinase-1,-2,-7 and -7) analysis. Histological analysis of cartilage of central and per-hipheral biopsies from patients with severe OA showed significant reduced number of chondrocytes in both superficial and middle zones. In the lower cartilage layer with severe structural lesions a cospicous number of cartilagineous repair-islands were noticed. Immunohistochemical analysis showed high levels of tenascin in all cartilage layers of byopses showing structural damages. Frequently we observed an altered distribution of fibronectin. Metalloproteinase-2 (constitutive) is present in all stages during coxarthritis. Metalloproteinase-9 (not constitutive) is expressed at the final stages suggesting an important late role. Obtained results show that metalloproteinases have a peculiar behaviour during coxarthritis vs. other pathologies. Costitutive metal-loproteinases have a fundamental role in extracellular matrix remodelling, MMP-2 especially.