At the London Osteoporosis Clinic, pharmacological treatment is always part of a broader clinical strategy — not the entirety of it. Drug therapy is prescribed only when a patient’s clinical assessment, bone density results, and fracture risk profile indicate that it is warranted, and it is always accompanied by appropriate nutritional and exercise support.
The guide below summarises the principal drug treatments used in osteoporosis management, how each works, and the patient profile for which it is most appropriate. It is intended to support informed conversations with your consultant — not to replace clinical guidance.
At the London Osteoporosis Clinic, medication is viewed as one component of a broader bone restoration and fracture prevention strategy. Treatment plans are tailored to the individual and may combine: consultant-led assessment, bone density monitoring, nutritional optimisation, resistance and balance training, Vitamin D and calcium assessment, and carefully selected pharmacological therapy.
For patients at higher fracture risk, treatment sequencing strategies may involve an initial bone-building (anabolic) phase followed by antiresorptive therapy to maintain gains. The objective is not simply stabilisation, but meaningful improvement in bone strength, fracture resilience, and long-term musculoskeletal capability.
Teriparatide works by intermittently stimulating PTH receptors to promote new bone formation — making it an anabolic therapy ideal for osteoporosis treatment.
In contrast, continuous high levels of natural PTH lead to bone resorption (a catabolic effect), regulating calcium balance but potentially causing bone loss if sustained.
Antiresorptive drugs slow or stop bone loss by inhibiting the activity of osteoclasts — the cells that break down old bone. They stabilise bone density and reduce fracture risk but do not directly stimulate new bone formation. They are the most widely prescribed first-line pharmacological treatment for osteoporosis.
UK Brands: Alendronic acid, Risedronate, Ibandronate
How it works: Bisphosphonates bind to bone mineral and inhibit osteoclast-mediated resorption, reducing the rate at which bone is broken down. They are effective at both spine and hip sites and reduce vertebral, non-vertebral, and hip fracture risk.
Administration: Oral weekly or monthly.
First-line treatment for most patients with osteoporosis.
UK Brand: Prolia®
How it works: A fully human monoclonal antibody that binds RANKL and prevents osteoclast formation, function, and survival. Produces bone density gains comparable to or exceeding bisphosphonates.
Administration: Subcutaneous injection every 6 months.
For patients intolerant to bisphosphonates.
UK Brand: Aclasta®
How it works: The most potent bisphosphonate, administered as an intravenous infusion. Reduces vertebral fracture risk by approximately 70%, non-vertebral fracture risk by 25%, and hip fracture risk by 41%.
Administration: IV infusion once annually.
For patients unable to adhere to oral regimens.
UK Brand: Evista®
How it works: Mimics oestrogen’s protective effects on bone in post-menopausal women, inhibiting bone resorption without stimulating breast or uterine tissue. Reduces vertebral fracture risk by approximately 30–50%.
Administration: Oral tablet, once daily.
Post-menopausal spinal osteoporosis or osteopenia.
Anabolic drugs stimulate new bone formation by activating osteoblasts — the cells that build bone. They can achieve meaningful increases in bone mineral density and are particularly appropriate for patients with severe osteoporosis, very low T-scores, multiple fractures, or inadequate response to antiresorptive therapy. Anabolic therapy is typically followed by antiresorptive treatment to consolidate the bone density gains achieved.
A synthetic fragment comprising the first 34 amino acids of parathyroid hormone. When administered by daily injection, the intermittent PTH receptor stimulation shifts the remodelling balance strongly toward bone formation — producing substantial increases in bone density, particularly in the spine.
Daily subcutaneous self-injection (max 24 months)
A monoclonal antibody that inhibits sclerostin, a protein that suppresses bone formation. By blocking sclerostin, romosozumab simultaneously increases bone formation (anabolic) and reduces bone resorption (antiresorptive) — producing rapid, large BMD gains at both spine and hip.
Monthly subcutaneous injection for 12 months
Osteoporosis management is rarely a single drug for life. For many patients — particularly those with severe bone loss or high fracture risk — the most effective strategy involves a planned sequence of treatments.
A typical sequential approach begins with 12–24 months of an anabolic agent (teriparatide or romosozumab) to stimulate new bone formation and achieve substantial BMD gains, followed immediately by antiresorptive therapy (usually a bisphosphonate or denosumab) to consolidate and maintain those gains. Without the antiresorptive follow-on, a significant proportion of the BMD gained during anabolic therapy is lost within 12–18 months.
The specific sequence, duration, and choice of agents is individualised to the patient’s clinical profile, treatment history, response to monitoring, and preferences. No two treatment plans at LOC are identical.
Every patient at LOC receives an individualised assessment integrating bone density, fracture history, clinical risk factors, lifestyle, and long-term goals.
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