Related Experiment Video
Updated: Aug 14, 2026

07:23
Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification
Published on: December 3, 2016
Periosteal hyperostosis resulting from prostaglandin therapy
European Journal of Radiology
|August 1, 1986
Summary
Lamellated cortical hyperostosis in premature infants can signal trauma or infection. However, long-term use of prostaglandin preparations to maintain ductus arteriosus patency can also induce this bone condition.
Area of Science:
- Neonatal medicine
- Pediatric radiology
- Skeletal dysplasias
Background:
- Lamellated cortical hyperostosis in infants typically suggests trauma, congenital infection, or Caffey disease.
- Prostaglandin preparations are increasingly used for prolonged periods to manage congenital heart conditions by maintaining ductus arteriosus patency.
Observation:
- A case study or review focusing on premature infants treated with long-term prostaglandin infusions.
- Radiographic evidence of bilaterally symmetric, marked diaphyseal periosteal new bone formation.
Findings:
- Long-term administration of prostaglandin preparations can induce lamellated cortical hyperostosis.
- This induced hyperostosis may mimic other pathological conditions, necessitating careful clinical correlation.
Implications:
- Clinicians should consider prostaglandin-induced periosteal new bone formation in the differential diagnosis of hyperostosis in infants receiving these medications.
- This finding highlights a potential iatrogenic effect of prostaglandin therapy, requiring awareness for accurate diagnosis and management.
- Further research may be warranted to elucidate the precise mechanisms and long-term consequences of this drug-induced bone change.
Related Concept Videos
Bone Remodeling
Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
Osteoclasts in Bone Remodeling
Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during bone...
Bone Disorders
Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Peptic Ulcer Disease IV: Management
Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current medication...
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current medication...

