Corticosteroids

Corticosteroids (glucocorticoids) are among the most powerful anti-inflammatory drugs in medicine. In orthopaedics they appear in two very different ways: as systemic therapy for inflammatory and autoimmune disease (where the orthopaedic surgeon usually sees the side effects rather than prescribes the drug), and as local injections into joints, bursae, and tendon sheaths to relieve pain.

For the exam, the key is to understand both the benefit (rapid, strong suppression of inflammation) and the harm, because corticosteroids are heavily examined for their musculoskeletal complications. Three threads recur throughout this topic: how they work, what they do to bone (glucocorticoid-induced osteoporosis and osteonecrosis - the two headline harms), and how to use them safely, both as an injection and around surgery.

Glucocorticoids are lipid-soluble and pass straight through the cell membrane. Inside the cell they bind the glucocorticoid receptor in the cytoplasm. The activated receptor-steroid complex then enters the nucleus and changes which genes are switched on and off.

The two ways they reduce inflammation:

• Switching off inflammatory genes (transrepression): the complex blocks transcription factors such as NF-kB and AP-1, so the cell makes fewer cytokines, fewer adhesion molecules, and less of the enzymes that drive inflammation.
• Switching on anti-inflammatory genes (transactivation): they increase production of proteins such as lipocortin (annexin A1), which inhibits phospholipase A2 and so reduces the release of arachidonic acid - the raw material for prostaglandins and leukotrienes.

The net effect is less inflammation, less immune activity, and less pain. Because the glucocorticoid receptor is present in almost every tissue, the same drug also affects bone, muscle, skin, blood vessels, glucose handling, and the immune system - which is exactly why the side-effect list is so long.

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Effects on bone (the orthopaedic core):

The osteocyte point is high-yield: unlike the gradual thinning of osteoporosis, osteocyte apoptosis is thought to disrupt the bone's ability to sense and repair damage, helping to explain why corticosteroids cause osteonecrosis and not just low bone density.

Relative anti-inflammatory potency runs dexamethasone greater than methylprednisolone greater than prednisolone greater than hydrocortisone. In general, the more potent and longer-acting agents have less mineralocorticoid (salt and water retaining) activity, which is why dexamethasone is favoured when fluid retention must be avoided.

Osteonecrosis of the Femoral Head

Corticosteroids are the most common cause of non-traumatic osteonecrosis, and the femoral head is the typical site. The bone dies through a combination of osteocyte apoptosis and impaired blood supply, the dead segment loses its ability to repair, and over time the subchondral bone collapses, leading to pain and secondary osteoarthritis. Early radiographs are often normal, so MRI is the key early investigation, and because the insult is systemic the disease is frequently bilateral.

Stopping and the Stress Response

Corticosteroids run through every part of orthopaedic practice and the exam. In clinic they are the everyday injection for an osteoarthritic knee, a painful shoulder, or a trigger finger - so the indications, technique, and limits of intra-articular steroid are practical knowledge. In basic-science vivas the mechanism of action and the way steroids damage bone are classic questions. In trauma and arthroplasty the recognition of osteonecrosis of the femoral head and the management of a steroid-dependent patient (impaired healing, infection risk, and stress-dose cover) are common scenarios. Knowing when steroids help, what they damage, and how to use them safely is the core that examiners probe.

• Glucocorticoid-induced osteoporosis guidelines (for example the American College of Rheumatology, and equivalent guidance from NOGG in the UK and other national societies) agree on the core principles: assess fracture risk early, give calcium and vitamin D to all long-term users, and add an antifracture drug (oral bisphosphonate is the usual first choice) for those at moderate or higher risk, with anabolic agents reserved for the highest-risk patients.
• Osteoarthritis guidelines (for example AAOS and NICE) place intra-articular corticosteroid as an option for short-term symptom relief, not as disease-modifying treatment, reflecting trial evidence that the benefit is temporary and that repeated injection may harm cartilage.
• Where guidance differs is mainly the threshold for starting bone-protecting drugs and the place of newer anabolic agents, rather than any disagreement on the underlying harm of long-term steroids.
• Global practice variation largely reflects drug availability and cost (for example the choice between oral and intravenous bisphosphonates or anabolic agents) rather than differences in the principles of safe corticosteroid use.