How does hyperparathyroidism cause bone weakening

The result of too much parathyroid hormone is that bones lose their density and hardness. If that wasn't bad enough, the excess calcium removed from the bones stays in your blood making you feel bad see our page on symptoms. If you have kidney stones and hyperparathyroidism--guess where the kidney stones came from? That's right, the calcium in the kidney stones came from your bones! The loss of calcium from bones is called osteoporosis.

Bones which have lost some of their calcium are said to be "osteoporotic". Osteoporotic bones are more likely to break. In fact, the definition of osteoporosis indicates that the likelihood of fracture is 10 times higher than normal. Yep, a fold increase in the incidence of fracture. If you have severe osteoporosis, the risk of fracture increases up to fold! The picture of the yellow bones above and to the right a bit shows a normal bone section on the bottom and a bone with osteoporosis on the top.

The osteoporotic bone has bigger holes in it as a result of the calcium being dissolved and put into the blood stream. Osteoporosis has 3 causes: 1 excess parathyroid hormone, 2 advanced age, and 3 lack of estrogen in older females.

This page is primarily about cause number one--osteoporosis due to parathyroid disease Osteoporotic bone is not as strong as regular bone and therefore, bones that have osteoporosis are much more susceptible to fractures. All patients with hyperparathyroidism will get osteoporosis if the parathyroid tumor is not removed This continued dissolving of the central bone is what causes the bone pain so common to hyperparathyroidism.

It is also what contributes to the weakening of the spinal column resulting in elderly persons walking "hunched over". The picture on the right shows what a normal bone left and an osteoporotic bone right look like under a microscope. You can see that the bone on the right is much less dense and has more open areas.

There is much less calcium structure that gives the bone its strength. The process of losing the calcium out of the bones is often felt as an aching pain in the bones hips, legs, wrists, and lower back usually.

Osteoporosis is seen very nicely in this picture. This is an actual photo of a broken hip bone from a man with osteoporosis due to a parathyroid tumor. The osteoporosis is seen as bone that is very thin. It actually looks weak and you can imaging how this bone is more prone to break than a normal bone that is thick and strong.

Patients with parathyroid tumors will get osteoporosis that is more severe than people without parathyroid tumors, and the osteoporosis develops faster than osteoporosis which is not associated with a parathyroid tumor. Remember, the drugs which have been developed for the treatment of osteoporosis Fosamax, Actonel, Evista, Boniva, Miacalcin, etc, are very good drugs for routine osteoporosis, but they were not designed to work in patients with parathyroid tumors, and they do not.

Let us say this again, taking Fosamax or Actonel or any other osteoporosis medicine will not help the osteoporosis in a man or woman who has a parathyroid tumor. The picture of the skeleton on the left shows in different colors where osteoporosis occurs most commonly and therefore, where people with osteoporosis are most likely to break a bone.

Note that the lower back, the hips, and the wrist are the most common places to break a bone if you have osteoporosis. If you don't address it, then you can end up bent over The test that is done to check the density of bones is called a "DEXA" scan. When you get a DEXA scan you will see that they check two main areas Now you know why. Our bones are at their strongest in our early 20's.

They stay at this level of strength for a number of years, but then begin to lose strength slowly when we are in our mid 30's. Once we hit mid-life, we all lose a little bone density, but this is most evident for women. Estrogens have a protective effect on bone density which becomes evident after menopause when women begin to lose calcium from their bones at a faster rate then men of the same age.

That is one of the reasons most doctors feel that most post-menopausal women should be on some form of estrogen therapy. If you are a woman then you probably know this is a little controversial, but the reason that estrogens are even considered is to protect the bones from the normal slow loss of bones. As you will learn later on this page, there is no medication for osteoporosis associated with hyperparathyroidism.

Estrogens will NOT help and will not slow down the process if you have a parathyroid problem. The parathyroid problem MUST be addressed. Please watch a 6-minute video of Dr Norman discussing this concept. This is a very popular and award-winning video. As you know from other pages of this web site, overactive parathyroid glands secrete too much parathyroid hormone.

The excess parathyroid hormone PTH has a direct effect on the bones To achieve this goal, more complex laboratory tests to monitor the bone turnover and imaging techniques and modalities as high-resolution peripheral quantitative computed tomography HR-pQCT and trabecular bone score TBS are employed.

These imaging techniques showed the affection of microarchitecture of the cortical and the trabecular bone. For the time being, surgery and alendronate treatment are believed to reverse the catabolic effect of hyperparathyroidism on the bone. Vitamin D supplementation in case of vitamin D deficiency may also has a protective effect on the skeleton. Over the last hundred years, the effect of parathyroid hormone PTH on bone metabolism was extensively discussed. PTH acts on the bone cells through several mediators, and its action involves a variety of cells.

It is now understood that parathyroid hormone has both catabolic and anabolic effects on bone metabolism [ 1 ]. Mandl in Austria was the first to prove that the enlarged parathyroid was responsible for the skeletal manifestations of hyperparathyroidism after the first successful removal of parathyroid adenoma [ 2 ]. This change in clinical presentation was accompanied by the introduction of newer lab tests to assess bone turnover and newer imaging techniques to assess the bone quality [ 2 ].

The treatment modalities also evolved, allowing more individualized approach for treating each patient [ 4 ]. The main function of PTH is to maintain calcium levels within the normal range thorough its action on the bone, kidneys, and intestine.

It also decreases serum phosphorous through inhibiting renal reabsorption [ 5 , 6 ]. PTH can produce catabolic or anabolic effect on bone metabolism depending on the level of the hormone, periodicity, and duration of exposure [ 6 , 7 ].

PHPT and cPTH enhance cortical bone loss by increasing osteoclastic activity but produce cancellous bone that is relatively preserved or modestly increased [ 2 , 9 , 11 ].

The pattern of bone loss in PHPT is different from the pattern of bone loss in osteoporosis. In osteoporosis, the trabecular bone loss predominates, while in PHPT the cortical bone loss predominates [ 14 ].

Normally, bone structural integrity is maintained by the process or remodeling where the bone is removed by osteoclasts and new bone is synthesized by osteoblasts [ 15 ]. The osteoclasts and osteoblasts are arranged in a structure called the basic multicellular unit BMU.

A BMU consists of osteoclasts in front with osteoblasts, some blood vessels, and connective tissue behind [ 16 , 17 ]. Osteoclasts are formed by fusion of mononuclear precursors, while osteoblasts originate from undifferentiated mesenchymal cells [ 16 , 18 ].

While osteoblasts, osteocytes, and lymphocytes, mesenchymal stromal cells express PPR, osteoclasts respond indirectly to PTH through various mediators and cytokines produced by cells which carry PPR [ 6 , 19 , 20 , 21 , 22 , 23 ]. It is now believed that osteocytes are the primary cellular target of PTH in the bone. Osteocytes are the main cells that express PPR in the musculoskeletal system [ 14 ]. Saini et al. These mice showed significant increase in bone mineral density BMD , reduced osteoblast activity, and decreased skeletal response to anabolic or catabolic PTH regimen [ 24 ].

Other studies also supported the fact that osteocytes rather than osteoblasts are the main source of the receptor activator of nuclear factor kappa-B ligand RANKL in the process of osteoclastogenesis [ 25 , 26 ]. Where mice lacking RANKL in osteocytes had less bone loss compared to control mice when they are exposed to dietary calcium deficiency for 30 days causing secondary hyperparathyroidism.

Another study was designed with a co-culture of osteoclast precursors and osteocytes. This ratio is decreased with parathyroidectomy PTx or medical treatment by alendronate [ 28 ]. This results in increased bone turnover, osteopenia, and bone loss in hyperparathyroidism. In addition, several extraskeletal manifestations of hyperparathyroidism are due to increased bone catabolism and hypercalcemia as nephrolithiasis, renal failure, peptic ulcer, and mental changes [ 2 ]. RANKL binds to the receptor activator of nuclear factor kappa-B RANK on the osteoclast precursor stimulating their differentiation to osteoclasts and on the surface of the osteoclasts increasing their bone-resorbing activity.

Cells of bone marrow also play a role in the effect of PTH on bone metabolism. Lymphocytes are believed to play a role on bone metabolism. T lymphocytes express PPR [ 23 ]. Th17 cells form a subset of T lymphocytes that contribute to bone resorption. This is consistent with a human study that showed statistically significant elevation of IL in postmenopausal women who had osteoporosis when compared with postmenopausal women who had osteopenia [ 47 ].

Thus, in these mice there was no cortical bone loss, and there was increased trabecular bone formation [ 19 ]. It also increases the expression of CD40 by stromal cells and osteoblasts increasing their responsiveness to CD40L expressed by T cells.

Bone marrow macrophages also play a role in the action of PTH on the bone. Macrophages express PPR. Depletion of the precursors of macrophages decreases the anabolic effect of iPTH [ 19 ]. The monocyte chemoattractant protein-1 MCP-1 which is a chemotactic factor for monocyte and macrophages is a mediator for PHT-induced bone resorption [ 6 ]. MCP-1 was proven to attract pre-osteoclast in in vitro studies, thus increasing bone resorption [ 53 ]. This suggests that the transient increase of bone resorption may be necessary before the anabolic effect of PTH on the bone [ 53 , 54 ].

After PTx, the levels of MCP-1 decreased significantly starting from 15 minutes following parathyroid adenoma removal [ 55 ]. Hyperparathyroidism was first described in by von Recklinghausen.

Nowadays, the classical presentation with osteitis fibrosa cystica and pathological fractures is rarely seen in developed countries. Currently, larger numbers of patients are being identified with neuropsychiatric or cardiac manifestation and laboratory studies in the USA and Europe [ 2 , 56 ]. In developing countries, the symptomatic form of PHPT was prevalent for a long time, but some countries as Brazil and China are having a shift toward the asymptomatic disease.

However, other countries as India, Iran, Saudi Arabia, and Thailand still have high prevalence of the symptomatic form of the disease with pronounced skeletal manifestations [ 56 , 57 , 58 ]. The signs and symptoms of severe bone disease include bone pain and pathologic fractures. Skeletal muscles are also affected by hyperparathyroidism where the patients have proximal muscle weakness and hyperreflexia [ 2 , 59 ].

Hyperparathyroidism is when your parathyroid glands create too much parathyroid hormone in the bloodstream. These glands, located behind the thyroid at the bottom of your neck, are about the size of a grain of rice.

The parathyroid glands produce parathyroid hormone. This hormone helps maintain an appropriate balance of calcium in the bloodstream and in tissues that depend on calcium for proper functioning. Two types of hyperparathyroidism exist. In primary hyperparathyroidism, an enlargement of one or more of the parathyroid glands causes overproduction of the hormone. This causes high calcium levels in the blood, which can cause a variety of health problems.

Surgery is the most common treatment for primary hyperparathyroidism. Secondary hyperparathyroidism occurs due to another disease that first causes low calcium levels in the body. Over time, increased parathyroid hormone levels occur. Hyperparathyroidism is often diagnosed before signs or symptoms of the disorder are apparent. When symptoms do occur, they're the result of damage or dysfunction in other organs or tissues due to high calcium levels in the blood and urine or too little calcium in bones.

Symptoms may be so mild and nonspecific that they don't seem related to parathyroid function, or they may be severe. The range of signs and symptoms include:. See your doctor if you have any signs or symptoms of hyperparathyroidism. These symptoms could be caused by any number of disorders, including some with serious complications.

It's important to get a prompt, accurate diagnosis and appropriate treatment. The parathyroid glands maintain proper levels of both calcium and phosphorus in your body by turning the secretion of parathyroid hormone PTH off or on, much like a thermostat controls a heating system to maintain a constant air temperature. Vitamin D also is involved in regulating the amount of calcium in your blood. Normally, this balancing act works well.

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