Paget's disease: nursing assessment, interventions, and NCLEX questions

LS
By Lindsay Smith, AGPCNP
Updated March 30, 2026

Paget’s disease of bone (osteitis deformans) is a chronic metabolic bone disorder characterized by abnormally accelerated bone remodeling. Osteoclast hyperactivity drives excessive bone resorption, triggering disorganized compensatory osteoblast activity. The result is structurally weak, highly vascularized pagetic bone that fractures easily and causes pain, deformity, and neurological complications. Paget’s disease is the second most common metabolic bone disease after osteoporosis, affecting roughly 2–3% of adults over 55 in the United States. Nurses encounter it primarily in orthopedic, medical-surgical, and neurology settings. Recognizing the clinical picture — elevated alkaline phosphatase, characteristic X-ray findings, and bone pain worse at night — and knowing how to administer and teach bisphosphonate therapy are the core nursing competencies tested in clinical practice and on NCLEX.

Fast-scan summary: key Paget’s disease facts

Parameter Key facts
Most common site Pelvis (most common), followed by femur, tibia, skull, spine, clavicle
Primary lab marker Alkaline phosphatase (ALP) — can be 10× or more above normal
First-line treatment Bisphosphonates — zoledronic acid (Reclast) IV preferred; alendronate oral alternative
Most common complication Hearing loss (8th cranial nerve compression at skull base)
Most common symptom Bone pain — deep, aching, worse at night
Feared malignant complication Osteosarcoma transformation (<1% of cases)
Key nursing priority pre-bisphosphonate Ensure adequate calcium and vitamin D status before therapy to prevent hypocalcemia

Pathophysiology: abnormal bone remodeling

Normal bone remodeling is a tightly coupled cycle — osteoclasts resorb old bone, osteoblasts lay down new bone, and the two processes remain in balance. In Paget’s disease, this coupling breaks down. Osteoclasts become hyperactive, resorbing bone far faster than normal and triggering a reactive osteoblastic response. The new bone formed is disorganized and structurally inferior: a mosaic pattern of woven and lamellar bone replaces the orderly parallel lamellar architecture of healthy cortical and trabecular bone. The pagetic bone is enlarged, hypervascular, and mechanically weak.

Three phases of disease

Phase Dominant cell activity X-ray appearance Clinical correlate
Lytic (osteoclastic) Osteoclast overactivity dominates "Blade of grass" advancing lytic lesion in long bones; "osteoporosis circumscripta" in skull Early disease; bone is soft and prone to bowing
Mixed Both osteoclast and osteoblast activity Cortical thickening, coarsened trabecular pattern Most symptomatic phase — pain, deformity, warmth
Sclerotic (blastic) Osteoblast activity dominates Dense sclerotic bone; "cotton wool" skull; "picture frame" vertebra Bone is enlarged and dense but brittle; fracture risk persists

Etiology

The exact trigger remains unclear. The leading hypothesis involves paramyxovirus exposure (measles virus or respiratory syncytial virus) in genetically susceptible individuals. Mutations in the SQSTM1 gene (encoding p62 protein, which regulates osteoclast signaling) are identified in up to 40% of familial cases. The disease has a geographic clustering pattern — historically higher rates in the United Kingdom, Western Europe, Australia, and New Zealand — which supports an environmental-genetic interaction model. The incidence has been declining in recent decades, possibly reflecting reduced exposure to environmental triggers.

Sites of involvement

Paget’s disease is typically monostotic (one bone affected) or polyostotic (several bones). The most commonly affected sites are the pelvis (most frequent), proximal femur, tibia, skull, lumbar and thoracic spine, and clavicle. The long bones of the upper extremity and the small bones of the hands and feet are rarely involved. Site involvement determines the clinical complication profile: skull involvement drives hearing loss and headache; tibial involvement causes bowing deformity; spinal involvement risks cord compression.

Clinical presentation

The majority of patients with Paget’s disease are asymptomatic at diagnosis. The condition is frequently discovered incidentally when an elevated alkaline phosphatase is found on routine bloodwork or when characteristic X-ray changes appear on imaging ordered for an unrelated reason.

Symptom or sign Mechanism Nursing significance
Bone pain — deep, aching, worse at night Periosteal stretching, increased vascularity, microfractures Most common symptom; assess with OLDCARTS; distinguish from arthritis pain
Bowing deformity of tibia ("saber shin") Weight-bearing forces deform weakened pagetic cortex Gait disturbance, fall risk; footwear and assistive device evaluation
Skull enlargement (increased hat size, frontal bossing) Osteoblastic expansion of calvarium Prompts cranial nerve assessment; may precede hearing loss
Warmth over affected bone Hypervascularity of pagetic bone increases local blood flow Document skin temperature bilaterally; differentiate from infection
Pathologic fractures ("chalk-stick" pattern) Transverse fractures through abnormal cortex, perpendicular to long axis High priority in fall prevention; see fractures nursing reference
Hearing loss Skull base enlargement compresses CN VIII (vestibulocochlear) at petrous temporal bone Most common neurological complication; establish audiometry baseline at diagnosis
Headache Skull expansion, increased intracranial pressure, or hydrocephalus Assess character and frequency; new or worsening headache warrants neurological evaluation
Spinal cord compression Vertebral enlargement narrows spinal canal; pagetic bone encroaches on cord or nerve roots Urgent: assess motor strength, sensory level, bladder/bowel function
High-output cardiac failure Severe extensive disease creates arteriovenous shunting through hypervascular bone, increasing cardiac output demand Rare; assess for signs of heart failure in patients with widespread disease
Secondary osteoarthritis Deformed pagetic bone alters joint mechanics at hip, knee, or ankle Common cause of functional decline; see osteoarthritis nursing reference

Diagnosis

Laboratory findings

Test Finding in Paget's disease Clinical use
Total alkaline phosphatase (ALP) Elevated — often 10× or more above upper limit of normal in active disease Primary screening and monitoring marker; see nursing lab values cheat sheet
Bone-specific ALP (BALP) Elevated; more specific than total ALP (unaffected by liver disease) Preferred when liver pathology may confound total ALP
P1NP (procollagen type 1 N-terminal propeptide) Elevated — reflects osteoblast activity (bone formation marker) Sensitive monitoring marker during treatment; tracks treatment response
NTX (N-telopeptide of type I collagen) Elevated — reflects osteoclast activity (bone resorption marker) Monitoring treatment response; normalizes within weeks of effective bisphosphonate therapy
Serum calcium Typically normal in ambulatory patients; hypercalcemia may develop with immobilization Monitor during immobilization; assess before and after bisphosphonate therapy
Serum phosphate Normal Helps differentiate from other metabolic bone diseases

Imaging

Modality Characteristic findings Clinical role
Plain X-ray Cortical thickening; coarsened trabeculae; "blade of grass" advancing lytic lesion (long bones); "cotton wool" skull (sclerotic nodules on lytic background); "picture frame" vertebra (cortical thickening of vertebral margins) First-line imaging; confirms diagnosis; identifies bowing and fractures
Bone scan (radionuclide scintigraphy) Intense focal uptake in affected bones; may show multiple sites Staging — determines extent of disease and identifies all affected sites at diagnosis
CT scan Cortical detail, canal narrowing, fracture assessment Spinal stenosis evaluation; surgical planning
MRI Soft tissue involvement, cord compression, marrow signal change Neurological complications; distinguish sarcomatous change from normal pagetic marrow
Bone biopsy Mosaic pattern of woven and lamellar bone; enlarged osteoclasts with nuclear inclusions Rarely needed for diagnosis; indicated when sarcomatous transformation is suspected (new mass, sudden pain escalation, fracture)

Sarcomatous transformation: Osteosarcoma arising in pagetic bone affects fewer than 1% of patients but carries a poor prognosis. Clinical warning signs are a new soft-tissue mass, sudden escalation of previously stable bone pain, and elevated serum LDH. Refer promptly for orthopedic oncology evaluation.

Treatment

Bisphosphonates: first-line therapy

Bisphosphonates inhibit osteoclast-mediated bone resorption, normalizing the accelerated bone turnover that defines Paget’s disease. The treatment goal is biochemical remission — normalization of ALP and bone turnover markers — which halts disease progression, reduces pain, and may prevent complications. For more on bisphosphonate pharmacology in the context of bone disease, see the osteoporosis nursing reference.

Drug Route and dose Key nursing considerations
Zoledronic acid (Reclast) IV infusion; 5 mg single dose over ≥15 minutes Preferred agent — most potent, longest remission (5+ years). Ensure adequate hydration before infusion (500 mL oral fluid or IV saline). Monitor for acute-phase reaction (flu-like symptoms, fever, myalgia) in the first 1–3 days after first infusion; managed with acetaminophen. Contraindicated if creatinine clearance <35 mL/min. Dental evaluation recommended before therapy.
Alendronate (Fosamax) Oral 40 mg once daily × 6 months Take with a full glass (6–8 oz) of plain water on an empty stomach. Remain upright (sitting or standing) for at least 30 minutes after taking. Do not eat or take other medications for 30 minutes. Esophageal ulceration and erosion risk if taken incorrectly. Monitor for GI complaints.
Risedronate (Actonel) Oral 30 mg once daily × 2 months Same oral administration requirements as alendronate (water, upright, fasting). Less GI irritation than alendronate in some patients. Monitor ALP at 3 months post-treatment.
Pamidronate IV infusion; 60 mg over 2–4 hours for 3 consecutive days Older IV option; used when zoledronic acid is contraindicated or unavailable. Infusion reaction monitoring. IV site assessment.

Calcium and vitamin D: mandatory co-therapy

Before initiating any bisphosphonate, ensure adequate calcium and vitamin D status. Bisphosphonates suppress osteoclast activity abruptly; without adequate calcium intake, the body draws calcium from other sources, producing symptomatic hypocalcemia. Standard supplementation is calcium 1,000–1,500 mg/day and vitamin D 800–1,000 IU/day. In patients with documented deficiency, higher repletion doses may be needed before starting bisphosphonate therapy.

Calcitonin: second-line

Salmon calcitonin (subcutaneous or intranasal) reduces bone turnover but is substantially less effective than bisphosphonates and produces tachyphylaxis over time. It is reserved for patients who cannot tolerate bisphosphonates. Nursing considerations include injection site rotation and watching for nausea.

Analgesic therapy

Bone pain is managed with NSAIDs (ibuprofen, naproxen) or acetaminophen. NSAIDs require GI and renal monitoring. Successful bisphosphonate therapy usually reduces pain as disease activity normalizes over weeks to months; analgesics bridge the interval until biochemical remission.

Surgical interventions

  • Joint replacement: Total hip or knee arthroplasty for secondary osteoarthritis when conservative management fails. Pre-operative bisphosphonate therapy is recommended to reduce vascularity of pagetic bone and limit intraoperative blood loss.
  • Decompression surgery: Laminectomy or canal decompression for spinal stenosis with progressive neurological deficit.
  • Fracture fixation: Intramedullary nail or plate fixation for completed chalk-stick fractures; prophylactic fixation may be considered for impending fractures at high-risk sites.

Nursing assessment and interventions

Pain assessment

Use OLDCARTS (Onset, Location, Duration, Character, Aggravating factors, Relieving factors, Timing, Severity) to characterize bone pain systematically. Pain in Paget’s disease is typically deep, aching, and worse at night — a pattern that distinguishes it from joint-origin arthritis, which tends to correlate with activity. Document pain severity (0–10 scale), location, and response to analgesics. Pain that suddenly worsens or changes character warrants urgent imaging to rule out fracture or sarcomatous transformation.

Neurological assessment

Skull and spinal involvement drive neurological complications. Perform a baseline assessment that includes:

  • Hearing: Ask about hearing changes; arrange audiometry baseline at diagnosis for any patient with skull or temporal bone involvement.
  • Vision: Assess for diplopia or visual field changes (rare — optic nerve compression).
  • Headache: Document frequency, character, and associated symptoms; new or escalating headache in skull Paget’s requires CT evaluation for hydrocephalus.
  • Cranial nerves: Screen CN VII (facial symmetry) and CN VIII (hearing, balance) at minimum.
  • Spinal involvement: Assess strength, sensation, reflexes, and bladder/bowel function; new weakness or urinary retention requires emergent evaluation for cord compression.

Fall risk and mobility

Tibial bowing, gait disturbance, deformity, and pathologic fracture risk all elevate fall risk. Conduct a formal fall risk assessment (e.g., Morse Fall Scale) and document. Implement standard fall precautions. Assess need for assistive devices (cane, walker). For patients with bowing deformity, custom orthotics or footwear modifications may improve gait stability. For the full fracture management and prevention framework, see the fractures nursing reference.

Skin temperature assessment

Hypervascularity of pagetic bone produces detectable warmth over affected areas. Palpate bilaterally and document asymmetric warmth. While this is expected in Paget’s disease, sudden marked increase in warmth with erythema and fever should prompt evaluation for superimposed osteomyelitis.

Bisphosphonate medication teaching

Oral bisphosphonates (alendronate, risedronate):

  1. Take first thing in the morning, on an empty stomach.
  2. Swallow with a full (6–8 oz) glass of plain water only — not juice, coffee, or mineral water.
  3. Remain fully upright (sitting, standing, or walking) for at least 30–60 minutes after taking.
  4. Do not eat, drink (except water), or take other medications for 30 minutes.
  5. Never crush or chew the tablet.
  6. Stop taking and report immediately if you develop difficulty swallowing, chest pain, or new or worsening heartburn — these may indicate esophageal injury.

IV zoledronic acid (Reclast):

  1. Drink at least 500 mL of fluid (water, juice) in the 2 hours before the infusion.
  2. Infusion runs over at least 15 minutes — do not exceed the rate.
  3. Common after first infusion: fever, flu-like aching, and myalgia (acute-phase reaction) typically beginning 24–48 hours post-infusion and resolving within 3 days. Acetaminophen is effective. Reassure the patient this is expected with the first dose and usually does not recur.
  4. Monitor for hypocalcemia signs (tingling, muscle cramps, tetany) in the 24–48 hours after infusion, especially if baseline calcium status was low.

Calcium and vitamin D teaching

Counsel patients to maintain adequate calcium intake (1,000–1,500 mg/day through diet and supplementation) and vitamin D (800–1,000 IU/day minimum). Reinforce that these supplements are needed alongside — not as an alternative to — bisphosphonate therapy. Abrupt calcium deficiency after bisphosphonate initiation causes hypocalcemia; the supplements prevent this. See the nursing lab values cheat sheet for normal calcium reference ranges.

Monitoring

  • ALP: Check every 3–6 months during active treatment. Normalization of ALP is the primary endpoint of therapy; expect a 50–75% reduction within 3–6 months of effective treatment.
  • Bone turnover markers (P1NP, NTX): More sensitive for early treatment response monitoring; NTX normalizes within weeks.
  • Calcium and vitamin D: Check levels before initiating bisphosphonate therapy; supplement to normal range before first dose.
  • Creatinine: Check before IV bisphosphonate administration; zoledronic acid is contraindicated if CrCl is <35 mL/min.
  • Hearing: Annual audiometric evaluation for patients with skull base involvement.

Complications

Complication Mechanism Incidence Nursing action
Pathologic fractures (chalk-stick type) Transverse fractures through weakened pagetic cortex, often with minimal trauma Common, especially tibia and femur Fall prevention; report sudden pain or inability to bear weight; emergency imaging
Secondary osteoarthritis Bone deformity alters joint loading at hip, knee, and ankle Common in patients with lower extremity involvement Pain management; mobility assessment; refer for orthopedic evaluation when conservative management fails
Hearing loss (sensorineural) CN VIII compression at petrous temporal bone as skull base enlarges; also cochlear bone involvement Most common neurological complication (30–50% with skull involvement) Audiometry baseline at diagnosis; annual testing; refer to audiology; assistive devices
Spinal stenosis Vertebral enlargement narrows canal; pagetic bone compresses cord or nerve roots Significant with lumbar or thoracic vertebral involvement Assess motor strength, sensation, bladder/bowel; emergent escalation for new neurological deficits
Osteosarcoma transformation Malignant transformation of pagetic osteoblasts; mechanism poorly understood <1% of patients with Paget's disease Watch for new mass, sudden severe pain, elevated LDH; refer immediately for oncology evaluation
High-output cardiac failure Extensive hypervascularity increases total arteriovenous shunting, raising cardiac output demand beyond compensation Rare; only with severe polyostotic disease Assess for dyspnea, peripheral edema, elevated JVP in patients with widespread disease; standard heart failure management
Hypercalcemia of immobilization Rapid calcium release from highly active pagetic bone when weight-bearing ceases Uncommon; most at risk during hospitalization or post-fracture immobilization Monitor serum calcium; encourage early mobilization; IV fluids if symptomatic hypercalcemia develops

Special considerations for nursing practice

Hearing loss: the priority complication

Hearing loss is the most commonly tested and most clinically significant neurological complication in Paget’s disease. Establish an audiometry baseline at diagnosis for every patient with skull or temporal bone involvement. Document hearing changes at every encounter. Because CN VIII compression is often irreversible once established, early detection and treatment of active disease is the best prevention. Counsel patients that effective bisphosphonate therapy may stabilize hearing but is unlikely to reverse established loss.

Fall prevention is non-negotiable

Tibial bowing, gait disturbance, lower extremity deformity, and the elevated risk of chalk-stick fractures combine to make patients with Paget’s disease high-priority for fall prevention interventions. Conduct formal fall risk assessments, implement bed alarm and call-light protocols, ensure non-slip footwear, and assess the home environment for hazards. Occupational therapy referral is appropriate for patients with significant deformity or mobility limitation.

Teaching priorities for discharge

  1. Take oral bisphosphonates with full water, upright, fasting — and stay upright 30–60 minutes.
  2. Take calcium and vitamin D supplements daily.
  3. Report chest pain, difficulty swallowing, or worsening heartburn immediately if on oral bisphosphonate.
  4. Report any sudden increase in pain, new weakness, hearing changes, or difficulty with bladder or bowel control.
  5. Fall prevention strategies: assistive device use, home modifications, footwear.
  6. ALP blood test schedule: every 3–6 months during treatment.

NCLEX-style practice questions

Question 1

A nurse is teaching a patient newly prescribed alendronate (Fosamax) for Paget’s disease. Which instruction is most important to prevent esophageal complications?

A) Take the medication with 4 ounces of orange juice to improve absorption B) Take the medication and immediately lie down for 30 minutes to rest C) Take the medication with a full glass of water and remain upright for 30–60 minutes D) Take the medication with the first meal of the day to reduce nausea

Answer: C

Rationale: Oral bisphosphonates such as alendronate can cause severe esophageal erosions, ulcerations, and strictures if they remain in contact with the esophageal mucosa. Taking the medication with a full glass of plain water (6–8 oz) and remaining fully upright for at least 30–60 minutes are required to ensure the tablet reaches the stomach and does not lodge in the esophagus. Option A is incorrect — orange juice (acid, calcium content) impairs absorption and may worsen esophageal irritation. Option B is the opposite of the correct instruction — lying down traps the tablet. Option D is incorrect — bisphosphonates must be taken on an empty stomach; food dramatically reduces absorption.

Question 2

A patient with Paget’s disease has a total alkaline phosphatase (ALP) level of 320 U/L (normal: 44–147 U/L). The nurse reviews the chart and notes zoledronic acid was administered 4 months ago. Which finding would indicate the treatment is working?

A) ALP has decreased to 180 U/L and continues to trend downward B) ALP remains at 320 U/L and bone pain is unchanged C) Bone scan shows new areas of uptake in the lumbar spine D) Serum calcium has risen to 10.8 mg/dL

Answer: A

Rationale: The primary goal of bisphosphonate therapy is normalization of ALP, reflecting suppression of abnormal bone turnover. A downward trend — even if not yet normal — at 4 months indicates the treatment is working. Full normalization may take 6–12 months. Option B reflects treatment failure or insufficient response. Option C indicates disease progression, not response. Option D (mild hypercalcemia) is not a treatment endpoint and may reflect immobilization or over-supplementation.

Question 3

A nurse is conducting a health history for a 72-year-old patient with Paget’s disease involving the skull. Which complication should the nurse specifically assess for during the physical examination?

A) Deep vein thrombosis B) Hearing loss C) Peripheral neuropathy D) Renal calculi

Answer: B

Rationale: Hearing loss is the most common neurological complication of Paget’s disease and results from compression of CN VIII (the vestibulocochlear nerve) as the skull base enlarges. Patients with temporal bone or skull base involvement are at high risk. A baseline audiometric assessment should be performed at diagnosis. DVT (A) and renal calculi (D) are not characteristic Paget’s complications (though immobilization hypercalcemia may occasionally contribute to calculi). Peripheral neuropathy (C) is not a primary Paget’s complication, though nerve root compression from spinal involvement can occur.

Question 4

Before administering IV zoledronic acid to a patient with Paget’s disease, the nurse reviews the pre-infusion orders. Which order is most important to verify has been completed before starting the infusion?

A) Metoprolol 25 mg PO administered B) Calcium 500 mg and vitamin D 400 IU PO administered C) Patient has voided within the past 2 hours D) Patient has been NPO since midnight

Answer: B

Rationale: Bisphosphonates suppress osteoclast activity rapidly and dramatically. Without adequate calcium status, this suppression of bone resorption can precipitate hypocalcemia. Calcium and vitamin D supplementation must be established before bisphosphonate therapy — and verified before IV zoledronic acid infusion — to prevent this. Option A (beta-blocker) is unrelated to bisphosphonate administration. Option C (voiding) is not an IV bisphosphonate requirement, though adequate hydration (not voiding status) matters. Option D (NPO) applies to oral bisphosphonates (empty stomach requirement), not to IV administration.

Question 5

A radiology report for a patient with known Paget’s disease describes a “cotton wool” appearance of the skull and a “picture frame” vertebra at L3. Which phase of the disease do these findings most likely represent?

A) Lytic (osteoclastic) phase B) Mixed phase C) Sclerotic (blastic) phase D) Malignant transformation

Answer: C

Rationale: The “cotton wool” skull (areas of sclerotic density on a lytic background), “picture frame” vertebra (dense cortical thickening outlining the vertebral body), and cortical thickening are classic radiographic signs of the sclerotic or blastic phase of Paget’s disease, in which osteoblastic activity dominates. During the lytic phase, the classic findings are “osteoporosis circumscripta” in the skull and an advancing “blade of grass” lytic lesion in long bones. The mixed phase shows a combination of lytic and sclerotic changes. Malignant transformation would present as a destructive lesion with soft tissue mass, not the diffuse sclerotic pattern described.

Question 6

A nurse is caring for a patient with Paget’s disease affecting the pelvis and femur. The patient reports sudden, severe pain in the right thigh after stepping off a curb. An X-ray shows a transverse fracture through the mid-femoral shaft with no rotational deformity. The nurse recognizes this as which type of fracture?

A) Spiral fracture from torsional force B) Compression fracture from axial loading C) Chalk-stick fracture through pagetic bone D) Stress fracture from repetitive microtrauma

Answer: C

Rationale: Chalk-stick fractures are a hallmark of Paget’s disease. They are transverse fractures that occur through weakened pagetic cortex, often perpendicular to the long axis of the bone, and can occur with minimal or low-energy trauma. The transverse pattern with minimal deformity is characteristic. Spiral fractures (A) result from rotational forces and are associated with non-accidental injury and falls with twisting mechanism — their pattern is oblique and helical, not transverse. Compression fractures (B) are associated with vertebral bodies and axial loading. Stress fractures (D) are the result of repetitive loading and appear on imaging as subtle linear cortical changes, not complete transverse breaks.