A talar dome lesion is an injury to the cartilage and underlying bone of the talus within the ankle joint. Osteochondral lesions of the talus (OLT) are those that affect the chondral and subchondral areas of the talus. These authors evaluate the effectiveness of procedures such as microfracture and arthroscopy, and recent innovations such as … Osteochondral Repair of Talus: Causes Leading To Osteochondral Lesions. A mid-medial osteochondral lesion of the talus is demonstrated on Fig. Recommendations to proceed with diagnostic arthroscopy of the right ankle for evaluation of the congruity of the articular surface with possible removal of osteochondral fracture versus repair either arthroscopically or open were discussed in detail. The aim of this study was to summarize all eligible studies to compare the effectiveness of treatment strategies for osteochondral defects (OCD) of the talus. Most researchers believe that a traumatic cause plays a pivotal role in the development of a vast majority of OLTs. The MRI confirmed osteochondral fracture of the anterolateral talus with mild displacement. Anterolateral (2), anteromedial (1), and accessory portals (3) are demonstrated on Fig. Immobilization of the ankle, medications, steroid injections and physical therapy are commonly tried but this often fails to relieve symptoms and surgery may be required. [] Although majority may be associated with trauma, some may develop insidiously. The presence of an osteochondral lesion may initially go undetected and may manifest many months after the initial ankle injury. The proportion of the patient population treated succes … . Talar dome lesions are usually caused by … INTRODUCTION. The treatment for an osteochondral defect of the talus is extremely varied and depends on the size of the defect … Treating osteochondral lesions of the talus can pose challenges and delayed diagnosis due to late presentation after an ankle sprain. [] This is a broad terminology that encompasses a variety of disorders including osteochondritis dissecans, osteochondral fractures, and osteochondral defects. The University Foot and Ankle Institute is one of the top foot and ankle centers in the world. Osteochondral lesions of the talus are a reasonably infrequent cause of long-standing ankle pain and stiffness and are often the result of a severe ankle sprain type injury. Osteochondral Defect of the Talus (OCLT) is a condition that involves the cartilage of the ankle joint – specifically the talus. The Traumatic Defects. Osteochondral Lesions of the Talus Sara Lyn Miniaci-Coxhead, MD Dr. Miniaci-Coxhead or an immediate family member serves as a board member, owner, officer, or committee member of the American Orthopaedic Foot and Ankle Society. Osteochondral lesion of the talus, (cartilage damage of the ankle) can occur from a traumatic fracture or ankle sprain when the bones in the ankle joint hit each other damaging the cartilage surface. 20 The treatment of talar OCDs is usually initiated with a nonoperative protocol. This chapter is adapted from Chao W, Freeland E, Dedini R: Osteochondral Lesions of the Talus in Chou LB, ed: Orthopaedic… The ankle joint is made up of three different bones (tibia, fibula, and talus). The unstable cartilage rim … Surgery to treat an osteochondral ankle lesion is a series of steps that usually starts with the least invasive technique, an arthroscope, as the last step of diagnosis before your surgeon progresses with whatever needs to be done to repair the top of your talus. A talar osteochondral defect (OCD) is a combined lesion of the subchondral bone and its overlying cartilage. A microfracture technique of osteochondral lesion of the talus is demonstrated. The causes of an OLT can be classified into traumatic and non-traumatic defects. . It is also called an osteochondral defect (OCD) or osteochondral lesion of the talus (OLT). 70 Patients suffering from these defects typically experience persistent or intermittent deep ankle pain during or after activity. “Osteo” means bone and “chondral” refers to cartilage. Electronic databases from January 1966 to December 2006 were systematically screened. 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