Bone erosions are one of the hallmarks in the diagnosis, prediction and follow-up in RA and other inflammatory rheumatic diseases, such as SpA, erosive hand OA and gout.
Osteoclast activation is the final pathway leading to bone destruction. Why bone erosions in RA occur by preference at the peri-articular regions of finger joints is unclear. The cortex at the finger joints is extremely thin and is, in the bare area, not covered by cartilage or periost, and is therefore easily susceptible for developing erosions. The classical outside-in hypothesis considers synovitis as the primary trigger, which attracts osteoclasts from the circulation, resulting in bone erosions at the bare area and beneath articular cartilage and secondary bone marrow edema (BME). In contrast, the inside-out hypothesis considers bone marrow involvement as the primary trigger. A first argument is the role of ACPA antibodies produced by B-cells: they are able to directly stimulate osteoclasts, are present more than 10 years before clinical RA, and, in subjects with ACPA, bone erosions occur before the clinical onset of arthritis. Second, peri-articular bone loss precedes the occurrence of erosions. Third, BME precedes clinical RA, predicts future erosions and consists of lymphocytic inflammatory infiltrates. Other hypotheses include the role of mechanical stress, as erosions are mostly found at the radial and ulnar site of MCP's, the main location of peri-articular entheses.
However, bone erosions are also frequently found in healthy controls (HC), using conventional radiography (CR), MRI, ultrasound (US) and high-resolution peripheral quantitative computer tomography (HRpQCT). In normal conditions, the only well documented peri-articular cortical breaks are blood vessels that perforate bone from the periost toward the bone marrow at the epiphyses, proximal and distal to the growth plate. These vascular connections enable a direct local communication between bone marrow and synovium. In the context of the above hypotheses, pre-existing vascular connections and angiogenesis stimulated by inflammation could predestine the occurrence of erosions at these pre-existing vascular channels.
In SpA, bone erosions are preceded by BME in the SI joints and at the entheses of the vertebrae and peripheral joints. Here the hypothesis is that mechanical stress at the entheses is a predilection site for inflammation and bone destruction. Again, the predictive value of the presence of BME for developing erosions suggests that inflammation in the bone marrow could precede the occurrence of erosions.
Currently, CR of the hands and feet are the gold standard for imaging bone erosions in RA in research and clinical practice settings. However, CR is less sensitive in detecting bone erosions than MRI, US and HRpQCT. In order to better understand the occurrence of bone erosions, the availability of high-resolution 3D imaging, such as HRpQCT, and other techniques, such as PET-scan using specific inflammation markers, will allow more insights in the above hypotheses and should be studied in prospective studies in RA and in other rheumatic diseases with risk of bone destruction.
Disclosure of Interest None declared