What is the etiology of Paget's disease?

The typical clinical manifestations of Paget's disease include bone pain, bone deformities (e.g., enlarged skull, bowed legs), and an increased risk of fractures due to the weakened and structurally abnormal bones. Joint pain and gastrointestinal disturbances are not primary features of Paget's disease.

a. Joint pain and stiffness: Joint pain and stiffness are more characteristic of arthritis or other joint-related conditions, not the primary clinical manifestations of Paget's disease.

b. Muscle weakness and fatigue: While Paget's disease can cause discomfort and reduced mobility, it is not primarily associated with muscle weakness and fatigue.

d. Gastrointestinal disturbances and weight loss: Paget's disease primarily affects bone structures, and gastrointestinal disturbances and weight loss are not typical clinical manifestations of the condition.

The underlying pathophysiology of Paget's disease involves increased bone turnover and disordered bone remodeling. Osteoclasts, the bone-resorbing cells, become overactive, leading to excessive bone resorption. Osteoblasts, the bone-forming cells, attempt to repair the resorbed bone, but their activity is disordered, resulting in the formation of structurally abnormal bone.

a. Decreased bone density due to calcium deficiency: This is the pathophysiology of osteoporosis, not Paget's disease. In Paget's disease, bone density can be normal or increased due to the disordered bone remodeling.

c. Excessive collagen production leading to bone deformities: Excessive collagen production is not a characteristic feature of Paget's disease. The condition primarily involves abnormal bone remodeling by osteoclasts and osteoblasts.

d. Autoimmune attack on osteoblasts causing bone destruction: Paget's disease is not an autoimmune disorder. The disease is characterized by increased bone resorption and disordered bone formation, not an immune-mediated attack on osteoblasts.