Related Experiment Video
Updated: Jun 17, 2026
08:43
Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Pathological Calcification and Ossification in Relation to Leriche and Policard's Theory
Proceedings of the Royal Society of Medicine
|December 9, 2009
Summary
Bone calcification and ossification are linked to blood supply. Abnormal bone density, seen in conditions like fractures and tumors, can indicate issues with vascularity and healing.
Area of Science:
- Orthopedic Pathology
- Skeletal Radiology
- Bone Metabolism
Background:
- The Leriche-Policard theories explain bone pathology related to blood flow.
- Bone density changes, such as decalcification and sclerosis, have significant radiological implications.
- Pathological calcification and ossification can occur in various soft tissues and bone structures.
Purpose of the Study:
- To elucidate the mechanisms of pathological calcification and ossification in bone and soft tissues.
- To correlate radiological findings of bone density with underlying pathological processes.
- To explore the relationship between vascularity, calcium metabolism, and bone/tissue formation.
Main Methods:
- Review of established theories on bone pathology (Leriche-Policard).
- Analysis of radiological signs of bone density changes (decalcification, sclerosis).
- Examination of pathological calcification and ossification in diverse tissues.
Main Results:
- Hyperemia leads to bone decalcification, while reduced blood supply causes sclerosis.
- Diminished vascularity in fibrous tissue promotes calcification; excess calcium with adequate blood supply and fibroblasts can lead to ectopic bone formation.
- Radiological findings like decalcification in disuse, infection, or neoplasms, and avascularity in sequestra are significant.
- Hyperemic decalcification is linked to delayed fracture union and other conditions.
- Anaemic sclerosis is associated with various bone diseases, including syphilitic and malignant conditions, and can lead to bone fragility.
- Pathological calcification affects tendons, tumors, and cartilages; ossification occurs in tendons and cartilages.
Conclusions:
- Blood supply is a critical determinant in bone decalcification, sclerosis, calcification, and ossification.
- Radiological assessment of bone density provides crucial insights into pathological processes.
- Understanding these mechanisms is vital for diagnosing and managing a range of skeletal and soft tissue disorders.
Related Concept Videos
01:40Bone 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.
01:31Osteoclasts 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...
01:29Bone 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...
01:24Bone Formation by Endochondral Ossification
Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
01:27Growth of Cartilage and Bone Tissue
Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
01:26Coronary Artery Disease II: Pathophysiology
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...