This article on Epainassist.com has been reviewed by a medical professional, as well as checked for facts, to assure the readers the best possible accuracy.

We follow a strict editorial policy and we have a zero-tolerance policy regarding any level of plagiarism. Our articles are resourced from reputable online pages. This article may contains scientific references. The numbers in the parentheses (1, 2, 3) are clickable links to peer-reviewed scientific papers.

The feedback link “Was this Article Helpful” on this page can be used to report content that is not accurate, up-to-date or questionable in any manner.

This article does not provide medical advice.


Secondary Bone Cancer: A Cause For Pathologic Fracture

What Is A Secondary Bone Cancer?

Fractures caused as a result of Secondary Bone Cancer are called pathologic fractures. Primary cancer of breast, prostate, lung, thyroid and renal spread to distant bone through blood or lymphatics. The distant spread of cancer to bone is known as bone metastasis. The cancer spread into the bone often results in pathologic fracture.

Secondary Bone Cancer

When the cancer cells spread from its primary source to the bones then this condition is termed as secondary bone cancer. The original location of the cancer is called the primary cancer. A secondary bone cancer develops when some cancer cells from the primary tumor break away from primary cancer. The cancer cells flow through the bloodstream or lymphatics to distant organ and settle down in the bones. The cancer cells following initial deposits into skeletal structure start growing and spreading within bone to form a new tumor. The distal secondary tumor is known as metastasis. The distant spread of primary cancer cells may involve single or multiple bones. The following primary cancer metastasizes or spreads to distant bone or skeletal system.

Types Of Metastatic Cancer

The cancer or tumor cells once lodged in bone starts multiplying within the infrastructure of the bones. The bone infrastructures are made of connective tissue, osteoblast and osteoclast cells. The persistent growth of metastatic tumor within the bone destroys the integrity of the infrastructure and makes it weak. The tumor cell stimulates either osteoblast or osteoclast cells. Osteoblast cells forms more bones and osteoclast destroys the bone.

Osteoblast Activated Metastatic Cancer- Some metastatic cancer cells stimulates the normal osteoblastic cells, which are present in normal bone. Osteoblast cell stimulates formation of new bone. The expansion of new bone often weakens the surrounding bone, which result in fracture.

Osteoclast Activated Metastatic Cancer- Metastatic growth of cancer cells in bone often stimulates osteoclast cell.1 The activation of osteoclast cells causes lytic lesions. Lytic lesion follows resorption of bone and destruction of bony infrastructure. The lesion often looks like osteoporotic lesions. The bone resorption follows weakening of the infrastructure and fracture.

How Does Metastatic Cancer Increase The Risk For Pathologic Fracture?

Fractures caused as a result of Secondary Bone Cancer following metastasis or spread from primary cancer are called as pathologic fractures. Following are the list of primary cancer, which increase the risk of pathologic fractures when spread in bone.

Breast Cancer: The metastatic of the bone caused by breast cancer is the most common cause of the pathological fracture. This risk magnifies as the duration of the metastatic cancer growing in bone increases. Patient suffering with Breast Cancer live longer and have a prolonged survival rate. Individuals suffering from breast cancer are at increased risk for metastasis and pathological fracture following bone metastasis. Research estimates that lytic lesions caused by activation of osteoclast cells tend to increase the risk of bone fracture.2 The bony metastases of the breast cancer also stimulates osteoblast cells in lesser degree resulting in new bone formation. Osteoblastic lesions are often seen in secondary bone metastasis of femur. The rapid growth of metastatic tumor bone weakens the surrounding normal bone resulting in fracture with abnormal twist and turn.

Prostate Cancer: This is also a common cause of Pathologic Fractures. Prostate Cancer usually results in blastic lesions,3 which usually do not increase the risk of fractures but these lesions tend to decrease the stiffness of bone making them prone to fracture. Additionally, hormone treatment modalities used for prostate cancer also make the bones weak and fragile. The weak bone may fracture during activities because of improper weight transmission.

Lung Cancer: This is an extremely aggressive form of cancer and usually people with this form of cancer do not survive long enough to have a pathologic fracture but this form of cancer produces lytic lesions which increase fracture risk if there is metastasis to the bones

Thyroid Cancer: This form of cancer has lytic lesions and the risk of fracture is dependent on the location of the lesions. Since people with thyroid cancer have a long survival rate hence they are at increased risk for pathologic fractures.

Renal Cancer: This form of cancer also increases the risk of pathologic fractures if there is metastasis to the bone.

Radiation Treatment Of Bone: Bone cancer is often treated with radiation treatment. Radiation itself causes weakening of the bone resulting in fracture.


  1. Biology of Osteoclast Activation in Cancer G. David Roodman University of Texas Health Science Center at San Antonio and Audie Murphy Veterans Administration Hospital, San Antonio, TX.
  2. T cells induce pre-metastatic osteolytic disease and help bone metastases establishment in a mouse model of metastatic breast cancer. Monteiro AC1, Leal AC, Gonçalves-Silva T, Mercadante AC, Kestelman F, Chaves SB, Azevedo RB, Monteiro JP, Bonomo A. PLoS One. 2013 Jul 18;8(7):e68171.
  3. Osteoblasts stimulate the osteogenic and metastatic progression of castration-resistant prostate cancer in a novel model for in vitro and in vivo studies. Hagberg Thulin M1, Jennbacken K, Damber JE, Welén K. Clin Exp Metastasis. 2014 Mar;31(3):269-83.
Pramod Kerkar, M.D., FFARCSI, DA
Pramod Kerkar, M.D., FFARCSI, DA
Written, Edited or Reviewed By: Pramod Kerkar, M.D., FFARCSI, DA Pain Assist Inc. This article does not provide medical advice. See disclaimer
Last Modified On:July 29, 2021

Recent Posts

Related Posts