I am a medical doctor, and I am presently doing my PhD in relation to bio-medical informatics at the University of Oslo, Norway.
Bone resorption is the process of braking down the bones into its mineral and collagenous constituents through a cellular mechanism. The process may be part of the normal regulation of minerals such as Calcium in the blood or it could also be due to a pathological or disease process, which accelerates the rate of bony breakdown. In order to explain the process of bone resorption, first, it is vital to understand the structure of a bone and its cellular constituents.
Structure and Cellular Constituents of a Human Bone
In general, the bones are formed of cells, non-mineral collagenous matrix and mineral deposits. Among the cells present in the bony matrix, some contributes towards the formation and maintenance of the bone while other cells facilitate breakdown of the same. The cells that supports the formation and the maintenance of a bone, includes cells such as ‘osteoblasts’ and ‘osteocytes’. The cell type, which facilitates break down of a bone, is the ‘osteoclasts’.
When looking at the cross section of a bone, the outermost layer is termed as the ‘cortical zone’ while the inner zone of the bone is given the name, ‘trabecular’ or ‘spongy’ zone. Furthermore, the periosteum and endosteum lines the bone surface and the trabacular spaces respectively. These two linings are rather thin and consist of vascular complexes to supply nourishment to the cellular elements.
The matrix of the bone, which is mainly constituted by collagenous material, gains its hardness due to the deposition of mineral salts. Among these minerals, calcium and phosphorus are the most significant and in the living bony tissues, they exist as hydroxyapatite.
The Initiating Factors for Bone Resorption
In a healthy individual, the bone formation takes place until adulthood and thereafter a process known as ‘re-modeling’ will take over. Re-modeling refers to the replacement of ‘old’ bone tissues with new ones. Thus, resorption is an essential part of maintaining required density of a particular bone.
At the same time, the calcium level in the body is also a determining factor on the resorption state of a bone. Thus, when the blood calcium levels decrease, the parathyroid gland in the neck region will detect the same and will initiate the secretion of ‘parathyroid hormone’ (PTH). PTH will accelerate the resorption process in order to replenish the reduced calcium level in blood.
Apart from these factors, certain disease processes such as psoriatic arthritis, lack of stimuli, disuse, and even the old age can accelerate the process of bone resorption.
However, in all these instances, a common finding of highly active ‘osteoclasts’ could be readily visible.
Characteristics of Osteoclasts
These cells contain multiple nuclei with abundant mitochondria and lysosomes, which indicates its ability to perform energy demanding work such as bone resorption. They reside near the outer edge of the bone just underneath the periosteum. This will facilitate osteoclasts the easy access to the mineral dense portion of the bone.
The Steps Involved In Bone Resorption
The process is initiated by the factors mentioned above and with any such stimulus, the number and the activity of osteoclasts will rise. This will be facilitated by various chemical messengers released at the site of immature forms of osteoclasts (preosteoclasts) in the bone matrix. During this first step, many preosteoclasts mature into osteoclasts, which are able to de-mineralize the bone.
Once activated, the osteoclasts can secrete various enzymes including collagenases that are capable of digesting the mineralized bone and its collagen. As a result of osteoclasts invading the periosteum, the densely mineralized bone will break into its constituents while minerals such as calcium gets released to the blood circulation.
Regulating Excess Bone Resorption
When the osteoclasts become highly active and appear abundant in the bony matrix, the most likely result would be an increased destruction of the bone at a rate higher than its formation. Thus, to prevent such overwhelming de-mineralization, the regulatory mechanism in the parathyroid gland is also sensitive to the rising levels of calcium. As such, if it detects the calcium levels to be too high, the secretion of parathyroid hormone will lessen and therefore the resorption process will lose its steam. However, in a disease state, this would not be the main mechanism regulating the bone resorption and therefore the control may not be sufficient to prevent continued bone destruction.
James Orr on July 01, 2019:
Fractured humorous on 3/15/19. Surgery two weeks later after swelling went down with an Intramedullary (IM) rod. Sling off at 4 weeks with light physical therapy and more intense physical therapy for next 4 weeks. X ray at 8 weeks showed fracture not starting to heal. Stopped therapy and added Sarmiento Clamshell Brace for 5 weeks, staying in home and not lifting arm. X ray at 13 weeks (last Friday) showed fracture had increased in size.
Why did this happen? Can it still heal?
Maggie Griess from Ontario, Canada on May 06, 2013:
This is very useful. Also this is an article I will read in depth more than once.
I always thought we needed to supplement with calcium as we aged for the bone only, but it seems more complex...we need the calcium in our blood so the PTH won't try to reabsorb bone to adjust blood levels of calcium. Fascinating. So glad I have been supplementing with calcium as I am aging! Hopefully I got that right?