Osteochondroma, the most common benign bone tumor, is a projection on the external surface of the bone, which can be sessile or pedunculated. 85% of osteochondromas present as solitary lesions, while 15% occur in the context of hereditary multiple exostoses (HME), a genetic disorder that is inherited in an autosomal dominant manner. Although often asymptomatic, symptoms may eventuate from compression of adjacent vessels or nerves, fractures, osseous deformities, bursa formation, or malignant transformation. Cartilage cap thickness >2 cm in adults or >3 cm in children as well as new onset of pain or growth, or rapid growth of the lesion, especially after the closure of the growth plate, might reflect cancerous transformation. Surgical resection is indicated for symptomatic lesions, complications, cosmetic reasons or malignant transformation. Excision of the tumor with free margin is the treatment of choice. Local recurrence is less than 2% if complete resection is achieved.

Osteoid osteoma, the third most common benign bone tumor, usually occurs in the cortex of long bones. It consists of a radiolucent nidus surrounded by reactive osteosclerosis. Generally, osteoid osteoma affects young males. Nocturnal pain that eases with salicylates or nonsteroidal anti-inflammatory drugs (NSAID) is the typical clinical presentation. Sometimes, it remains undiagnosed for a long time. Plain radiography and computed tomography are usually sufficient for the diagnosis of osteoid osteoma. Initial treatment includes salicylates and NSAID because the tumor often regresses spontaneously over 2-6 years. Surgical treatment is indicated in case of unresponsive pain to medical therapy, no tolerance of prolonged NSAID therapy due to side effects, and no willingness to activity limitations. Nowadays, minimally invasive techniques have replaced open surgery and are considered the gold standard of surgical treatment. Although cryoablation seems superior in terms of the nerve damage and immunotherapy effect, radiofrequency ablation is the preferred technique.

Cellular senescence, a cell state characterized by a generally irreversible cell cycle arrest, is implicated in various physiological processes and a wide range of age-related pathologies. Oxidative stress, a condition caused by an imbalance between the production and the elimination of reactive oxygen species (ROS) in cells and tissues, is a common driver of cellular senescence. ROS encompass free radicals and other molecules formed as byproducts of oxygen metabolism, which exhibit varying chemical reactivity. A prerequisite for the generation of strong oxidizing ROS that can damage macromolecules and impair cellular function is the availability of labile (redox-active) iron, which catalyzes the formation of highly reactive free radicals. Targeting labile iron has been proven an effective strategy to counteract the adverse effects of ROS, but evidence concerning cellular senescence is sparse. In the present review article, we discuss aspects of oxidative stress-induced cellular senescence, with special attention to the potential implication of labile iron.