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: 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. The bone-density side is developed further in osteoporosis.

The conditions for which the injection is given each have their own page: subacromial impingement, trigger finger, de Quervain tenosynovitis, carpal tunnel syndrome and lateral epicondylitis — as does the disease that most often puts a patient on long-term systemic steroids in the first place, rheumatoid arthritis of the hand and wrist.

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.

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Relative anti-inflammatory potency runs dexamethasone greater than triamcinolone and 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.

Equivalent doses — learn these, because the rest of the page depends on them

⚠️ This table is not optional detail. The perioperative section below defines who needs stress cover in prednisolone (more than about 5 mg/day) but gives the doses in hydrocortisone — and the patient in front of you may be on dexamethasone or methylprednisolone. Without the conversion the protocol cannot be applied, and "steroid equivalence" is a stock viva question in its own right.

⭐ The single anchor worth memorising is hydrocortisone 20 = prednisolone 5 = methylprednisolone 4 = dexamethasone 0.75. From that one line you can convert any patient onto the stress-cover threshold and back again. Note the pattern the table makes obvious: as potency and duration rise, mineralocorticoid activity falls — which is why hydrocortisone is the agent for adrenal replacement (it supplies both glucocorticoid and mineralocorticoid effect) while dexamethasone is chosen when you want anti-inflammatory action without salt and water retention.

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.

How common is it? Give the number, because it is the reason for the low threshold to scan. Glucocorticoid-induced osteonecrosis develops in 9 to 40 percent of patients receiving long-term therapy (PMID 22169965). That is a very wide band, and it is worth being able to say why: the figure depends on the cumulative dose and peak daily dose, the underlying disease (series in lupus and transplantation sit at the high end, and the disease itself carries risk), and above all on how hard the study looked — cohorts screened with MRI find asymptomatic lesions that symptom-triggered radiographic series never count. Quote it as a range and name the reason for the spread; a single figure here would be false precision.

⭐⭐ Two points from the same source that change practice and are routinely missed:

• Osteonecrosis can occur WITHOUT glucocorticoid-induced osteoporosis. The two headline bone harms are dissociated — so a normal DEXA scan offers no protection and no reassurance against osteonecrosis, and a patient whose bone density has been checked and treated is not thereby screened for it. They are different lesions of different cells on different timescales: osteoporosis is a quantitative loss of bone driven by suppressed osteoblasts, osteonecrosis is death of osteocytes in a segment of bone.
• Bisphosphonates have a role in established osteonecrosis, not only in preventing the osteoporosis. Current evidence indicates they may rapidly reduce pain, increase ambulation and delay joint collapse in patients who already have osteonecrosis (PMID 22169965) — a useful adjunct to mention alongside protected weight-bearing when the head has not yet collapsed, though it does not displace core decompression or arthroplasty as definitive treatment.

Stopping and the Stress Response

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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.