User:Pathophysiology

Osteoporosis

Jackie is a 72 year-old who, last month, visited her granddaughter on her birthday. During the party, Jackie lifted her granddaughter onto her lap and felt a sharp pain in her back. After 3 days of rest, Jackie visited the doctor as the pain was still persistant. The doctor took some x-rays as well as a blood test and found out that she had a compression in one of her vertebraes.

Osteoporosis is the thinning of the bone. This means that the bone density becomes lower until it falls below 2.5 standard deviations of the peak bone mass which can lead to higher chances of bone fracture. It affects 1 in 37 Canadians, mostly in people above the age of 40. It is four times more common in women then it is in men. The most common bones affected are those of the hips, wrists, and spine. If a vertebrae in the spine is affected, it is compressed and it can cause the patients to become shorter. Most people get diagnosed when they experience a sharp pain in their back that has showed up for no reason or if they break a bone from falling or being hit, even if the impact didn't feel hard enough to break a bone.

      A person can get bone loss several ways. It can be due to heredity (smaller bone structure=higher risk), aging, lack of exercise, another illness, or low calcium, vitamin D, and phosphorus intake. It is strongly related to having lower than normal levels of estrogen in the body. Estrogen helps to maintain bone strength so without it, they can get weaker. Some medications, such as corticosteroids, can also lead to osteoporosis because they can affect how calcium gets absorbed in the body.

Pathophysiology To understand better the pathophysiology of osteoporosis one needs to understand how bone forms in naturally in our body. Generally, the bone is divided into two layers. The first, being the cortical bone, which constructs the outer layer of the bone and secondly, the spongy inner layer called the trabecular. Bone is not forever-young, thus it becomes damaged and cracked over time and must continuously undergo repairs. In bone injury, the trabecullar layer is most affected because of its larger surface area and higher metabolic rate than found in cortical bone. The bone comprises of a “remodeling process” which consist of continuous bone reabsorption and subsequent bone reformation. It is comprised of multi-cellular units of osteoclasts and osteoblasts. Osteoclasts are cells which reabsorb old and damaged bones while osteoblasts manufacture new ones. A Receptor activator of nuclear factor kappa B ligand (RankL) is located on the osteoblast that binds to the (Rank) receptor site on the osteoclast precursor, initiating the activation of osteoclasts. Osteoproteggerin, (OPG), is the protein released by osteoblast cell binding to (RankL) on the osteoclast and acts as a decoy blocking both (Rank) and (RankL) bonding. Within the remodeling process, reabsorption occurs first by osteoclasts adhering to the bone which then removes old and damaged cells by acidification and preoteolytic digestion. After reabsorption has been complete osteoblasts then secrete osteoid which later mineralizes into new bone. The formation phase (osteoclasts) takes longer than the reabsorption phase (osteoblasts). This takes approximately three weeks and three to four months to form bone respectively.

In osteoporosis, the remodeling process is altered. That is, new bone synthesis, osteoblasts, is slower than bone reabsorption, osteoclasts. Hence, in the disease osteoporosis bone reabsorption happens at a greater rate than bone formation. An example of a hormone which creates a high turnover reabsorption rate is the hormone estrogen. In post menoposal women, it is apparent that when there is a loss of estrogen in the body it may lead to introduced cytokines which then produces immature to mature osteoclast proliferation. Thus, inhibiting apoptosis allowing the continue eating of the bone. Another example is in found in elderly people. It is observed that there is a lower turnover time which slows down the process of bone formation due to limited number of osteoblasts or more commonly, the discontinued function of osteoblast due to aging.