Bone Marrow Oedema Syndrome

Abstract

Bone marrow ischaemia, osteochondral lesions and microfractures lead to an inflammatory response reaction in the epi- and metaphyseal region. Macrophages, monocytes and osteoclast precursors located in the bone marrow react with a release of cytokines and proinflammatory mediators leading to a capillary leak of the bone vessels followed by fluid outflow into the bone marrow interstitial space. Increased blood flow, reduced venous outflow and lymphocyte invasion further aggravate the bone marrow oedema (BME). Histological findings show fibrovascular regenerates and increased bone turnover with increased osteoclast activity. The bone marrow is hypocellular with oedema in the interstitial space and present lymphocytosis, plasmacytosis and fine fibrosis. Sinusoids show dilatation and disruption of their walls (capillary leak). Osteoclast activation leads to bone resorption and microfracturing of trabeculae. Bone mineralisation rate is reduced, but without marked loss of bone mass, as in the case of osteoporosis. The presence of active, intact bone cells is responsible for the repair capacity and the reversibility of the bone marrow oedema syndrome (BMES) after correction of the activated bone turnover. Increased fluid pressure and inflammatory mediators within the bone compartment activating the afferent nerves in the bone marrow cause the typical pain. In experimental studies the normal intraosseous pressure was found to be 20–30 mmHg. The increased bone turnover with increased osteoclastic activity due to an intraosseous inflammatory reaction with a capillary leak leads to fluid accumulation in the bone marrow interstitial space.