Pathophysiology Of Osteoporosis (How Osteoporosis Develops – In Layman’s Terms)

The Pathophysiology of Osteoporosis

Pathophysiology of Osteoporosis | Bone Remodeling | Chronic Inflammation Promotes Bone Loss  | The Bottom Line

Pathophysiology—unhealthy bone remodeling—occurs when bone removal outpaces bone formation

Pathophysiology, the medical discipline that describes what happens when normal physiology goes awry, seeks to explain what went wrong and why. In terms of your bones, pathophysiology occurs (#1) when the bone removal process is happening too quickly for the bone replacement process to keep up and/or (#2) when the bone replacement process is inhibited or has ground to a halt.

#1 Virtually anything that promotes chronic inflammation promotes excessive bone removal.

Examples include the many pro-inflammatory factors in the Standard American Diet; environmental exposures to a variety of pollutants, including pesticides, fluoride, heavy metals (lead, mercury, cadmium, arsenic), and endocrine disrupting chemicals, such as bisphenol A and phthalates. (1-14)

#2 The bone replacement process is blocked by anti-resorptive drugs, such as the bisphosphonates (e.g., Fosamax) and denosumab (i.e., Prolia, Xgeva), which shut down the bone removal process.

The bisphosphonates poison osteoclasts, the specialized cells that remove damaged or worn out bone, while denosumab prevents osteoclasts from even developing. Both inhibit new bone formation because old or damaged bone must be removed before new bone can be laid down.

Bone renewal is greatly hindered when the nutrients required to build new bone aren’t there in sufficient supply. Just as you can’t make an omelet without eggs, you can’t build bone without calcium, vitamin D, vitamin K2, vitamin C, magnesium, boron and a number of other trace minerals. In addition, a number of other nutrients, including the omega-3 essential fatty acids, vitamin A, vitamin E and the B vitamins play important roles in our ability to maintain healthy bones.

Bone pathophysiology is called osteopenia when the result is bone-thinning (osteo=bone, penia= decrease, deficiency), and osteoporosis, when so much bone has been lost that the bones (osteo) have become brittle and riddled with tiny pore-like holes (porosis). Both diseases indicate that the normal bone remodeling process has become imbalanced, so that bone-breakdown (bone-resorption) is outpacing bone formation.

Bone Remodeling Is Essential Throughout Life

Constant, balanced bone remodeling is essential for the maintenance of a healthy skeleton throughout life.

Healthy bone remodeling is normal, not pathophysiology — our bones are preprogramed to constantly rebuild themselves.

Your skeleton is not simply a static framework to which your muscles are attached. Your bones are very much alive and active, and are constantly remodeling themselves. In fact, 10% of your skeleton is removed and replaced each year – in 10 years, your entire skeleton will have created itself anew! (15)

This constant bone remodeling is normal physiology. You can’t maintain a healthy skeleton without it for the following reasons:

  • First, like all other cells, the cells that make up your bones get old and worn out, and need to be replaced with healthy new cells.
  • Secondly, even the normal activities of daily living put stress on our bones and cause tiny areas of damage that require replacement. For example, when you eat, your jawbones take a surprisingly heavy hit with every bite, so continuous removal and replacement of bone damaged by chewing is essential. Exercising and being active is great for our bones and stimulates new bone formation, partly by causing micro-damage to bone. When you dash down or up a flight of stairs, go for a walk, jog, play tennis, take a Zumba, Pilates or barre class, you create super tiny cracks in your bones that must be repaired. This constant repair and renewal is normal human physiology; these processes are supposed to be happening to maintain healthy bones.

Balance between the activities of the osteoclasts, the specialized cells whose job is to break down (resorb) old damaged bone, and the osteoblasts, the specialized cells that form new bone, is the key to bone health. The remodeling actions of both types of cells — the osteoclasts and the osteoblasts — are required for the maintenance of a healthy skeleton.  When osteoclast activity is prevented – as it is by the bisphosphonates and denosumab (the anti-resorptive drugs) — old damaged bone accumulates, gradually rendering bones fragile and increasing risk of fracture. When the nutrients that osteoclasts require to lay down new bone are not provided by the diet and supplements — or are not well absorbed due to compromised digestive function or are not well utilized due, for example, to chronic liver or kidney disease — osteoblasts’ ability to create healthy new bone is significantly impaired.

What happens in the bone remodeling process

Remodeling begins when inflammatory cell signaling triggers the development and activity of osteoclasts, which are attracted to areas of microfracture. Once there, the osteoblasts release hydrogen ions, via the activity of an enzyme osteoclasts’ contain called carbonic anhydrase. This acidifies the area, dissolving the mineralized bone matrix. While the bone matrix is dissolving, osteoclasts release several hydrolytic enzymes (e.g., cathepsin and matrix metalloproteases) that effectively break apart (digest) the chemical bonds holding together the organic components of the bone matrix.

The osteoclast demolition crews are normally done with their bone resorption work in just 2 weeks, after which the body begins to switch gears.  Just preparing osteoblasts to take over takes about 2 more weeks, following which new bone formation, which takes at least 13 weeks, begins. Just like remodeling a house, it takes a lot longer to rebuild than to break down bone. (For a hilarious visual, watch the demolition crew destroy a house in a matter of hours, then rebuild it over many months in the movie, The Money Pit, starring Tom Hanks and Shelly Long. Warning: If you are in the middle of remodeling your home, you may find this movie too true to life to be funny.)

It’s important to understand that the two aspects of the bone remodeling process, bone resorption and formation are not separate, independent processes. (16)

Osteoclasts and osteoblasts work together inside a unique temporary structure called the basic multicellular unit (BMU). Each BMU contains a team of osteoclasts in the front, a team of osteoblasts in the rear, a central capillary/blood vessel, a nerve supply, and associated connective tissue. In healthy human adults, 3–4 million BMUs are produced each year with ~1 million operating at any moment!

The average lifespan of the BMU osteoclast-osteoblast team is called “the remodeling period.” When all systems are functioning in proper balance, a full cycle of both aspects of the remodeling process is completed in 3–6 months. (17)

Each BMU begins at a particular place and time (origination) and advances toward a target, which is a region of bone in need of replacement, and for a variable distance beyond its target (progression), and eventually comes to rest (termination).

In cortical (also called compact) bone, which is the hard outer shell portion of your bones, the BMU travels through the bone, excavating and replacing a tunnel. In trabecular (also called cancellous) bone, which is the interior, spongy bone, the BMU moves across the surface, excavating and replacing a trench.

If your bones were M&M candies, cortical bone would be the hard outer shell and trabecular bone, the chocolate interior.

Actually, trabecular bone is more like the interiorPathophysiology of Osteporosis -Cortical vs Trabecular Bone of a Kit Kat Bar. It’s a meshwork of spongy tissue (called trabeculae) that makes up the inside of our vertebrae (the bones of the spine) and the ends of the long bones (e.g., the femur). Trabecular bone’s structure is a honeycomb of interconnecting spaces containing bone marrow, and this bone marrow is the source of the precursor bone cells that can grow up to become osteoblasts and orchestrate the formation and growth of new bone.

In both cortical and trabecular bone, the osteoclasts and osteoblasts in BMUs normally maintain a well-orchestrated spatial and temporal relationship with each other. As noted above, osteoclasts remove damaged bone by secreting acid and proteolytic enzymes that break down the bone matrix. As the BMU team advances, osteoclasts leave the resorption site, and osteoblasts move in to cover the excavated area and begin the process of new bone formation by secreting osteoid, an unmineralized, secretion of proteins that eventually gets mineralized into new bone.

The lifespan of each BMU is 6–9 months, which is much longer than the lifespan of either its osteoclasts or osteoblasts. So, a continuous supply of new osteoclasts and osteoblasts is essential for the BMUs to keep making progress on the bone surface.  Plus, we want the supply of new osteoclasts to be balanced by the supply of osteoblasts to get the bone-rebuilding work done.

Osteoblasts and osteoclasts are both derived from precursor cells in red bone marrow, which is found in the core of most bones. Osteoblasts are derived from precursor cells called mesenchymal stem cells (MSCs), while osteoclasts develop from precursors called hematopoietic stem cells (HSCs). MSCs can become either osteoblasts or adipocytes (fat cells). HSCs can become osteoclasts, immune cells (macrophages, neutrophils, basophils, eosinophils, T cells, B cells, natural killer cells) or platelets (a component of blood that prevents us from bleeding out by clumping together to form a blood clot).

Production of sufficient osteoclasts is not a problem. Inflammatory signaling triggers osteoclast production, and we certainly don’t have a deficiency of inflammation! Osteoblasts are the cell type modern man (and woman) are at risk of lacking.

What makes MSCs become osteoblasts and not fat cells?

MSCs make the decision to become osteoblasts and build bone for you when you are consuming enough of the (anti-inflammatory) omega-3 essential fatty acids to balance your intake of the (pro-inflammatory) omega-6 fatty acids. Balance here translates to a ratio of omega-6 to omega-3 of no more than 4:1.(18-22)

The omega-3s are alpha linolenic acid [ALA], for which the richest food source is flaxseed, and EPA and DHA, for which the richest dietary source is cold water fish, such as sardines and salmon.  EPA and DHA, in addition to causing MSCs to choose to become osteoblasts, are highly-anti-inflammatory.

The omega-6s are linoleic acid [LA], which is found in most vegetable oils (e.g., canola, corn, sunflower and soy oils), and therefore in most processed foods, and arachidonic acid [AA], which is present in significant amounts in meats, in dairy products from non-organic, grain fed cows, and in farm-raised fish.(23)(24)

In contrast to the omega-3s, the omega-6, AA, is highly inflammatory – and anything that promotes chronic inflammation promotes bone loss. Here’s why.

Chronic Inflammation Promotes Bone Loss

Inflammation triggers osteoblasts (yes, your bone-building cells) to produce a protein called the RANK ligand (RANKL). RANKL is an acronym for “receptor activator of nuclear factor-kappa B ligand.” (Fortunately, you don’t have to remember this. Just knowing the acronym RANKL is enough.) Once produced by osteoblasts in response to inflammatory conditions, RANKL zips over to the osteoclast precursor cells in your bone marrow and binds to the RANK receptor on the surface of these cells. This tells these osteoclast-precursors it’s time to start maturing into full blown osteoclasts.(25)

Pathophysiology of osteoporosis - inflammationRANKL is expressed in lots of tissues, not just by osteoblasts in your bone marrow. RANKL is expressed by cells in your muscles, thymus, liver, colon, small intestine, adrenal gland, breasts, prostate and pancreas. Why, you might ask – because RANKL to RANK binding also triggers the production of your immune defender T cells. Another name for RANKL is “tumor necrosis factor ligand superfamily member 11” because RANKL’s binding to RANK tells your body to produce immune cells that destroy cancerous tumors and invading viruses, unfriendly bacteria and other pathogens.(26)(27)

How does RANKL-RANK binding send the “get going” message to your osteoclasts and immune cells?

When RANKL binds to its cell surface receptor, RANK (receptor activator of nuclear factor-kappa B, another long name you don’t need to remember), this turns on a seriously pro-inflammatory messenger called NF-kappa B (nuclear factor-kappa B). NF-kappa B moves from the cell membrane into the cell and makes a beeline for its DNA, where it sets off the production of a whole bunch of pro-inflammatory processes—one of which is the activation of osteoclasts. When RANKL activates the RANK receptor on the precursor cells for osteoclasts, these osteoclast-hopefuls get the message that they are to develop into mature osteoclasts and remove worn out, damaged or infected bone.

Too much RANKL secretion, however, promotes bone loss. So, what can you do to prevent it?

If you choose to go the pharmaceutical route, you can take the anti-resorptive drug, denosumab (marketed as Prolia and Xgeva), which prevents bone remodeling by binding to and preventing RANKL from doing its job, thus preventing osteoclasts (but also your immune cells, specifically your T cells) from maturing and doing theirs.

RANKL can be controlled safely, naturally

A more intelligent way of preventing excessive RANKL secretion is dealing with its cause: chronic inflammation!

In addition to our modern diet, aptly called the SAD (Standard American Diet), which promotes inflammation in numerous ways — including delivering far too much omega-6 and far too little omega-3 (the omega-6: omega-3 ratio of the SAD is 20:1!) — many other environmental and lifestyle factors in our lives promote osteoclast-activating, bone-busting inflammation. (And you can expect to hear more about them, and how to avoid them, in future blogs.) A key factor discussed in this post is that just improving your omega-6: omega-3 ratio can go a long way towards putting out any chronic inflammation smoldering in your body, and the increase in RANKL-RANK binding it promotes.

Another action you can take is to increase your body’s production of RANKL’s natural decoy, another protein produced by osteoblasts called osteoprotegerin. Osteoprotegerin (OPG) also binds to RANKL, effectively preventing RANK-RANKL binding. In contrast to the drug, denosumab, however, our natural OPG does not completely shut down osteoclast formation and activity, but allows necessary healthy bone remodeling (and immune cell maturation!) to continue.(28)

How can we encourage our natural production of OPG?

By consuming vitamin K and soy foods. Vitamin K, in both its vitamin K1 and vitamin K2 forms, promotes a healthy balance between RANKL and OPG. Vitamin K1 lowers inflammation and RANKL, while K2 (MK-7) increases OPG. Whole soy foods contain a bioactive isoflavone (a phytonutrient compound) called genistein, which lowers inflammation, in part by increasing production of OPG and decreasing that of RANKL.(29-32)

The Bottom Line:

The pathophysiology of osteoporosis /osteopenia is the result of an imbalance between bone resorption by osteoclasts and bone formation by osteoblasts. Unfortunately, many factors in our modern Western lifestyle can disrupt the healthy balance between these two cell types that is required for lifelong bone renewal. The healthy balance between osteoclast and osteoblast activity can be upset by anything that causes the inflammatory cell signaling that triggers osteoclasts into motion to be chronically activated — or by hampering osteoblasts’ ability to lay down new bone by blocking the bone removal process or by not providing the nutrients needed.

The solution is not to prevent all osteoclast activity (as do the anti-resorptive drugs, the bisphosphonates and denosumab), but to restore balanced bone remodeling. This is done by

  1. Identifying, in each individual person, the specific inflammatory factors that are promoting excessive osteoclast activation and controlling or eliminating them.
  2. Ensuring bones’ nutrient needs are met, so osteoblasts are provided with an optimal supply of all the nutrients they require to build new bone.

Sources:
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  12. Fardellone P, Séjourné A, Paccou J, et al. Bone remodelling markers in rheumatoid arthritis. Mediators Inflamm. 2014;2014:484280. doi: 10.1155/2014/484280. Epub 2014 Apr 15. PMID: 24839355
  13. Arends S, Spoorenberg A, Brouwer E, et al. Clinical studies on bone-related outcome and the effect of TNF-α blocking therapy in ankylosing spondylitis. Curr Opin Rheumatol. 2014 May;26(3):259-68. doi: 10.1097/BOR.0000000000000053. PMID: 24625371
  14. Arends S, Spoorenberg A, Bruyn GA, et al. The relation between bone mineral density, bone turnover markers, and vitamin D status in ankylosing spondylitis patients with active disease: a cross-sectional analysis. Osteoporos Int. 2011 May;22(5):1431-9. doi: 10.1007/s00198-010-1338-7. Epub 2010 Jul 6. PMID: 20603707
  15. Wheeless C. Bone remodeling. Wheeless’ Textbook of Orthopaedics. Duke University. http://www.wheelessonline.com/ortho/bone_remodeling, accessed 5-6-2016.
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  19. Poulsen RC, Moughan PJ, Kruger MC. Long-chain polyunsaturated fatty acids and the regulation of bone metabolism. Exp Biol Med (Maywood). 2007 Nov;232(10):1275-88. PMID: 17959840
  20. Kruger MC, Coetzee M, Haag M, et al. Long-chain polyunsaturated fatty acids: selected mechanisms of action on bone. Prog Lipid Res. 2010 Oct;49(4):438-49. doi: 10.1016/j.plipres.2010.06.002. Epub 2010 Jun 17. PMID: 20600307
  21. Kelly OJ, Gilman JC, Kim Y, et al. Long-chain polyunsaturated fatty acids may mutually benefit both obesity and osteoporosis. Nutr Res. 2013 Jul;33(7):521-33. doi: 10.1016/j.nutres.2013.04.012. Epub 2013 Jun 10. PMID: 23827126
  22. Kajarabille N, Díaz-Castro J, Hijano S, et al. A new insight to bone turnover: role of ω-3 polyunsaturated fatty acids. ScientificWorldJournal. 2013 Nov 4;2013:589641. doi: 10.1155/2013/589641. PMID: 24302863
  23. Komprda T, Zelenka J, Fajmonová E, et al. Arachidonic acid and long-chain n-3 polyunsaturated fatty acid contents in meat of selected poultry and fish species in relation to dietary fat sources. J Agric Food Chem. 2005 Aug 24;53(17):6804-12. PMID: 16104803
  24. Kouba M, Mourot J. A review of nutritional effects on fat composition of animal products with special emphasis on n-3 polyunsaturated fatty acids. Biochimie. 2011 Jan;93(1):13-7. doi: 10.1016/j.biochi.2010.02.027. Epub 2010 Feb 25. PMID: 20188790
  25. Armour KJ, Armour KE. Inflammation-induced osteoporosis. The IMO model. Methods Mol Med. 2003;80:353-60. PMID: 12728730
  26. Aubin JE, Bonnelye E. Osteoprotegerin and its ligand: a new paradigm for regulation of osteoclastogenesis and bone resorption. Osteoporos Int. 2000;11(11):905-13. PMID: 1119324
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  28. Malan J, Ettinger K, Naumann E, Beirne OR. The relationship of denosumab pharmacology and osteonecrosis of the jaws. Oral Surg Oral Med Oral Pathol Oral Radiol. 2012 Dec;114(6):671-6. doi: 10.1016/j.oooo.2012.08.439. PMID: 23159111
  29.  Marini H, Minutoli L, Polito F, et al. OPG and sRANKL serum concentrations in osteopenic, postmenopausal women after 2-year genistein administration. J Bone Miner Res. 2008 May;23(5):715-20. doi: 10.1359/jbmr.080201. PMID: 18433304
  30. Sasaki N, Kusano E, Takahashi H, et al. Vitamin K2 inhibits glucocorticoid-induced bone loss partly by preventing the reduction of osteoprotegerin (OPG). J Bone Miner Metab. 2005;23(1):41-7
  31. Koshihara Y, Hoshi K, Okawara R, et al. Vitamin K stimulates osteoblastogenesis and inhibits osteoclastogenesis in human bone marrow cell culture. J Endocrinol. 2003 Mar;176(3):339-48. PMID: 12630919
  32. Wu W, Kim M, Ahn B. Inhibitory effect vitamin K on RANKL-induced osteoclast differentiation and bone resorption. Food Funct., 2015,6, 3351-3358 DOI:  10.1039/C5FO00544B

Lara Pizzorno

5 thoughts on “Pathophysiology Of Osteoporosis (How Osteoporosis Develops – In Layman’s Terms)

Donald

My mother has to take a regular maintenance dose of 10 milligrams Prednisone every other day for her lupus I know that prednisone is probably not a good thing for helping to rebuild her bones but she has to take it nevertheless so I guess my question now would be is there any hope that the algaecal plus will be able to help her given the fact that she must take the prednisone to control her lupus?

Lara Pizzorno

Hi Donald,

Yes, unfortunately prednisone, along with other glucocorticoid medications (e.g. Prednisolone, Kenalog, Dexamethasone) causes bone loss. These drugs cause bone loss via a number of different mechanisms. The gluccocorticoid drugs:
· Suppress the activity of our bone-building osteoblasts, while, at the same time, leave the number of bone-resorbing osteoclasts either unchanged or slightly increase their production.
· Induce production of caspase 3 and other proteins that play key roles in cellular apoptosis (cell-suicide), causing apoptosis in both osteoblasts and osteocytes (what osteoblasts become after they begin secreting the bone matrix). Because osteocytes play a central part in skeletal sensing of the need for bone repair and also in the bone repair process, this results in weakening of bone (within 6 months) even when glucocorticoids are used at very low doses
· Change the balance between receptor activator for NF-κB ligand (RANKL) and osteoprotegerin (OPG). As explained in this post on the Pathophysiology of Osteoporosis, RANKL, which is generated by osteoblasts and osteocytes, is a key regulator of osteoclast recruitment, activation, and survival. Osteoblasts and osteocytes also produce OPG, which is a decoy receptor for RANKL and thus inhibits its actions on osteoclasts. The balance between RANKL and OPG is a central determinant of more (RANKL) or less (OPG) bone resorption; glucocorticoids tip this balance in favor of RANKL.
· Cause an increase in the production of macrophage colony-stimulating factor, a pro-inflammatory cytokine that triggers the production of more pro-inflammatory cytokines. Inflammation promotes the generation of osteoclasts.
· Furthermore, glucocorticoids also directly prolong the lifespan of mature osteoclasts.
· Inhibit Wnt protein expression in mature osteoblasts, which results in the precursor cells of osteoblasts (mesenchymal progenitor cells) becoming adipocytes (fat cells) instead of osteoblasts.
· Deplete vitamin D3.

The end result of all this is that bone mineral density (BMD) drops 6-12% within the first year of glucocorticoid use, and approximately 3% per year following. Fracture risk escalates up to 75% within the first 3 months.

If your mother must take a glucocorticoid drug, her bones need all the help you can provide. She needs to do everything she can to optimize her bones’ ability to rebuild – this definitely includes taking AlgaeCal Plus and Strontium Boost. And because prednisone depletes vitamin D, I would also recommend having her blood levels of 25(OH)D checked (this is the form in which vitamin D circulates in the bloodstream. Her levels should be in the 50-80 ng/mL range. The 30 ng/mL level, which you may see listed as adequate is not adequate for your mother – or anyone else for that matter – 29 ng/mL is widely considered insufficient. So, who wants to be just barely better than downright insufficient?

Because glucocorticoids promote mesenchymal stem cells’ choosing to become adipocytes rather than osteoblasts, your mother also needs to be supplying her bones with optimal amounts of omega-3 essential fatty acids, specifically, EPA and DHA, as these omega-3s promote the development of osteoblasts from MSCs and lessen inflammation as well. And it is very important that she do all she can to lessen inflammation. For these reasons, she should also be taking Triple Power, which will supply her with the EPA/DHA she needs along with 2 highly anti-inflammatory natural agents: curcumin and astaxanthin.
She should be eating a whole –organic—foods diet both because the levels of many nutrients and anti-inflammatory phytonutrients are far higher in organically grown foods (and dairy and meat from pastured animals, and eggs from free range chickens, and wild caught rather than farmed fish) AND to minimize her exposure to the pesticide residues found in conventionally produced foods, which promote inflammation.

Providing optimal support for her bones’ healthy renewal will absolutely and greatly help minimize the bone loss caused by prednisone.

Seibel MJ, Cooper MS, Zhou H. Glucocorticoid-induced osteoporosis: mechanisms, management, and future perspectives. Lancet Diabetes Endocrinol. 2013 Sep;1(1):59-70. doi: 10.1016/S2213-8587(13)70045-7. Epub 2013 Jun 28. PMID: 24622268
Davidge Pitts CJ, Kearns AE. Update on medications with adverse skeletal effects. Mayo Clin Proc. 2011 Apr;86(4):338-43; quiz 343. doi: 10.4065/mcp.2010.0636. Epub 2011 Mar 9. PMID: 21389249

– Lara

Mary Ann Rogers Kowbuz

I have Osteoporosis and have avoided the Biophosphonates all my life. At age 82 I am till ambulatory with mechanical assistance. These notes are so appreciated. Looking for help as doctors only promote pharmaceuticals that are counterproductive. Thank you very much.

Mary Ann Rogers Kowbuz

I have Osteoporosis and have avoided the Biophosphonates all my life. At age 82 I am till ambulatory with mechanical assistance. These notes are so appreciated. Looking for help as doctors only promote pharmaceuticals that are counterproductive. Thank you very much. I am taking Warfarin. Just received first Prolia. What can I do?

Monica

Hi Mary,

AlgaeCal Plus and Strontium Boost are clinically proven (and guaranteed) to increase bone density, naturally. They provide you with the nutrients your bones need: organic plant-based calcium, magnesium, vitamin K2, vitamin D3, boron and over 70 trace minerals. You can see the research here: https://www.algaecal.com/research/ and the hundreds of success stories here: https://www.algaecal.com/expert-insights/tag/success-stories/

You may also find the following articles helpful:
https://www.algaecal.com/expert-insights/vitamin-k-only-safety-issue-warfarin/
https://www.algaecal.com/expert-insights/denosumab-aka-prolia-xgeva-even-worse-than-the-bisphosphonates/

– Monica from AlgaeCal

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