Pathophysiologie und aktuelle Behandlungskonzepte bei ausgewählten Osteonekrosen

Zusammenfassung

Osteonekrosen treten sowohl beim heranwachsenden als auch ausgewachsenem Skelett meist an prädisponierenden Lokalisationen mit Bevorzugung der Epiphysen auf. Pathophysiologisch unterscheidet man neben einer idiopathischen Form zwischen einer primär vaskulären (Thromboembolien, Hämoglobinopathien usw.) und einer toxischen (Cortison, Alkohol, Chemotherapeutika usw.) Genese. Unabhängig der Ätiologie resultiert eine Nekrose der Knochentrabekel und des angrenzenden Knochenmarks sowie eine Ödembildung. Durch avaskuläre Umbauvorgänge bildet sich eine Fibrose und mechanisch instabiler Geflechtknochen aus, sodass es im Verlauf zu einer subchrondralen Fraktur und einem Gelenkkollaps kommt. Insbesondere bei Beteiligung großer Gelenke resultieren sekundär arthrotische Deformitäten, sodass insbesondere die Hüftkopfnekrose sowie die fokale subchondrale Osteonekrose und Osteochondrosis dissecans des Knies von klinischer Bedeutung sind. Diagnostisch ist neben der nativ-radiologischen Röntgendiagnostik die Magnetresonanztomographie mit der charakteristischen Darstellung des „Sichelzeichens“ entscheidend. Therapeutisch können als konservative Maßnahmen lediglich periphere Vasodilatatoren oder Bisphosphonate als off-label use Schmerzen reduzieren und die Zeit bis zum Gelenkflächenkollaps verhindern, wohingegen die hyperbare Sauerstofftherapie, die Stoßwellentherapie, Antikoagulanzien und Statine allgemein nicht angewendet werden sollten. Die Standardtherapie in frühen Stadien ist die retrograde Anbohrung mit der Zielsetzung einer Ödementlastung und einer Unterbrechung der Sklerosezone zur Revaskularisation. Weitere operative Maßnahmen wie Umstellungsosteotomien, vaskularisierte Knochentransplantate sowie Knorpelplastiken sind möglich, wobei diese mit dem prothetischem Gelenkersatz konkurrieren.

Abstract

Osteonecrosis occurs in both children and adults with the main focus on the epiphysis as a predisposed location. Pathophysiologically, a distinction is made between primary vascular (thromboembolism, haemoglobinopathy etc.), toxic (alcohol, cortisone, chemotherapeutic agents) and idiopathic origin. Independently of the aetiology, osteonecrosis leads to necrosis of the bone trabeculae and the adjacent bone marrow as well as oedema formation. Avascular remodelling causes fibrosis and the formation of mechanically unstable woven bone, leading to a subchrondral fracture and a collapse of the joint surface. Especially if large joints are involved, secondary osteoarthritic deformities occur, so femoral head necrosis, focal subchondral osteonecrosis and osteochondrosis dissecans of the knee are of clinical significance. X-ray and MRI are crucial diagnostic procedures. The treatment of osteonecrosis is challenging. For conservative therapy, the off-label use of peripheral vasodilators and bisphosphonates may reduce pain and time to articular collapse, whereas hyperbaric oxygen therapy, shockwave therapy, anticoagulants and statins are not recommended. Standard treatment in early stages focuses on retrograde drilling aimed at reducing oedema and breaking down the sclerosis zone to establish a process of revascularisation. Further operative options such as corrective osteotomies, vascularized bone grafts and cartilage remodelling surgery are possible, but they compete with prosthetic joint replacement and are inferior, especially in progressive stages.

Schlüsselwörter

Osteonekrosen - Femurkopfnekrose - fokale subchondrale Nekrose - Osteochondrosis dissecans - Talusnekrosen

Key words

osteonecrosis - femoral head necrosis - focal subchondral necrosis - osteochondrosis dissecans - talus necrosis

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