# The Potential of Indole Alkaloids in Bone Health and Osteoporosis Management  
[PERSON]  
1 Department of Science, University of Basilicata, Vale dell'Ateneo Lucano 10, 85100 Potenza, Italy;  
[EMAIL_ADDRESS]
2U.O.S. Reunatalogia, P.O. of Castrovillari, ASP Cosenza, 87012 Castrovillari, Italy; [EMAIL_ADDRESS]  
[PERSON]  
2U.O.S. Reunatalogia, P.O. of Castrovillari, ASP Cosenza, 87012 Castrovillari, Italy; [EMAIL_ADDRESS]  
[PERSON]  
3 Faculty of Science, Assiut University, Assiut 71516, Egypt; [EMAIL_ADDRESS]  
[PERSON]  
1 Department of Science, University of Basilicata, Vale dell'Ateneo Lucano 10, 85100 Potenza, Italy;  
[EMAIL_ADDRESS]  
Footnote 12: email  
testosterone in men can accelerate bone loss. Inadequate calcium and vitamin D intake, lack of weight-bearing exercise, and smoking can increase the risk. Certain medications, such as corticosteroids and some cancer treatments, can weaken bones. Conditions like rheumatoid arthritis, hyperthyroidism, and celiac disease can contribute to osteoporosis. Bone tissue, like muscle, skin, and blood, is not a static and inert structure, but a living and highly metabolically active tissue that renews itself under physiological conditions through a metabolic process called bone remodeling [1; 2]. Unlike static tissues, bone is a dynamic organ undergoing constant remodeling through a balanced process of bone resorption and formation. A decrease in the size of the thoracic and abdominal cavities as well as an increase in thoracic kyphosis can result from vertebral fractures, which can also cause discomfort and postural abnormalities that can lower quality of life overall. Up until a fracture occurs, the condition is clinically asymptomatic [3; 4]. Osteoporosis is a health and social problem; it affects in Italy 14% of men over 60 and 23% of women over 40. Its frequency is rising, but the majority of cases are still undiagnosed and untreated [5]. Due to a complex pathophysiology, resorption outweighs new production in the two stages of bone remodeling, resulting in an imbalance [6]. The primary causes include a shortage of calcium and vitamin D, loss of sex hormones, and neglect. The decrease in sex hormones is exponentially correlated with bone loss. The typical loss of lumbar spine bone density in the first year following menopause is 8%; this decreases to half in the subsequent years and reaches a plateau approximately five years later. Postmenopausal bone loss occurs at such a fast pace that it causes trabecular bone perforation and irreversible skeletal tissue loss [7; 8]. The thinning and perforation of the trabeculae lead to a progressive loss of connectivity between the trabeculae, which is the source of the change in skeletal microarchitecture seen after menopause and during aging. The porotic bone has the characteristic 'palisade' radiographic look because the horizontal trabeculae, which are not under direct load, are the first to weaken and disintegrate. An exponential rise in bone fragility occurs when the horizontal trabeculae vanish [9; 10; 11]. Because there is no physical foundation for new bone production, trabecular perforation causes irreversible bone loss. In other words, the resorbed bone cannot be replaced by new bone. In actuality, the physiological function of osteoblasts is to fill the trabecular pits that they create with the bone matrix, which will subsequently calcify. Even if the osteoblastic activity is elevated, no bone is created because trabecular perforation leaves no cavity for the osteoblasts to deposit the matrix on [12; 13; 14; 15; 16; 17; 18; 19; 20; 21; 22]. Bone growth, maintenance of skeletal mass, and subsequent bone loss occur as a result of continuous resorption and new formation processes, known as bone remodeling (Figure 1). This is the process in which old bone is replaced by new bone. There are two main types of cells responsible for bone remodeling: osteoclasts, which are responsible for bone resorption, and osteoblasts, which are responsible for bone formation.