Our bones operate in a balanced and dynamic system, which in the normal situation keep them strong. Bones are constantly being eliminated and then remade to keep them healthy and read to support our frame.
This normal process involves two major kinds of bone cells that work together, in balance, to keep bones healthy and strong.
There are cells that lay down new bone called osteoblasts. Then there are cells that break down the old bone called osteoclasts.
Cancer cells can affect bones in two different ways.
1- One of these ways is through a process that the cancer cells make substances that turn on the osteoclast cells leading to the bone being broken down without new bone being laid down. This process weakens the bones and often develops holes in the bone that are called osteolytic or lytic lesions. Lytic lesions become weak and can eventually lead to bone to fractures with little or no trauma to the body.
2- In the alternative the cancer cells release substances that turn on the osteoblast cells causing new bone to be laid down without old bone first being broken down. When this happens there becomes areas of the bones that become harder, a condition called sclerosis. These sclerosis areas in bones are called osteoblastic or blastic lesions. Contrary to what seems reasonable, these harder blastic areas actually break more easily than normal bone.
Both of these types of metastasis can cause pain. Actually, bone metastasis is one of the most frequent causes of pain in people with cancer, including advanced prostate cancer.
In cases where the cancer spreads to the bones of the spine, it can press on the spinal cord causing nerve damage that may even progress to paralysis if not treated.
Another common occurrence is that when the cancer cells damage the bones calcium is released from the bones into the blood. These increased calcium levels can lead to problems caused by high blood calcium levels (hypercalcemia).
Bone metastases are serious and must be treated in order to avoid unnecessary pain and serious complications.
Joel T. Nowak