The aim of this talk is to provide insights into recent advances in the fields of secondary osteoporosis and emerging anti-osteoporotic therapies.
There are several diseases and medications which may cause secondary osteoporosis. Among most prominent causes are rheumatic diseases such as rheumatoid arthritis, ankylosing spondylitis, but also polymyalgia rheumatica and giant cell arteritis (GCA). For example, new study data demonstrate a clear association between GCA and several conditions known to be related to glucocorticoid use including osteoporosis. As a matter of fact, glucocorticoids remain to be among the most important and most frequently used anti-inflammatory and immunosuppressive or immune-modulatory acting drugs to treat rheumatic (and other) diseases. And indeed, glucocorticoids also exert undesired effects, especially if higher dosages have to be given over longer periods of time. In this regard, glucocorticoid-induced osteoporosis (GIOP) and other adverse effects are to be mentioned here. However, the available data describing frequency and severity of these adverse effects are fragmentary. For example, it is difficult to distinguish specific adverse effects of a glucocorticoid therapy from other causations (e. g., the treated disease itself, other concomitant diseases or concomitant therapies). This statement is especially true for GIOP in the context of chronic inflammatory rheumatic diseases.
Current anti-osteoporotic therapies mainly consist of medications such as bisphosphonates, denosumab, selective estrogen receptor modulators and teriparatide. However, there are promising drugs currently in development which use the recent advances in our knowledge of bone biology. Examples to be discussed here comprise both antiresorptive medications such as cathepsin-K inhibitors (odanacatib) and anabolic agents such as antisclerostin monoclonal antibodies (romosozumab and blosozumab) or PTHrp 1-34 (abaloparatide).
Disclosure of Interest None declared
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