Aspirin is a cyclooxygenase inhibitor that is extensively used to prevent cardiovascular disease and cancer. Aspirin has been dubbed a “miracle medicine” for decades. It is easy to see why; it is an analgesic. It can lower a fever. It can lower the risk of stroke and heart attack in patients who are predisposed to cardiovascular problems, as well as the risk of some malignancies. It is cheap, simple to make, and readily available without a prescription.
In recent years, studies have linked aspirin use to improved bone health and a lower incidence of bone fractures following falls (which can have devastating consequences, especially among older adults). A new study is now looking into the potential benefit to bones. Its consumers are the elderly, who are prone to osteoporosis. It also suppresses the creation of prostaglandin E2, which is necessary for bone remodeling. This raises the question of whether it can affect bone health in users. The purpose of this review was to summarise the available literature on the effects of aspirin on bone health.
Using major scientific databases, a literature search on experimental and clinical evidence on the effects of aspirin on bone health was conducted. Aspirin has been shown in vitro to increase the survival of bone marrow mesenchymal stem cells, and the progenitors of osteoblasts, and to induce the development of preosteoblasts. Aspirin also blocked the nuclear factor kappa-B (NFB) pathway and lowered the production of receptor activators of NFB ligand, which inhibited osteoclast development.
In osteoporosis animal models, aspirin helped reduce bone loss. Despite having a beneficial effect on bone mineral density, aspirin did not reduce fracture risk in human epidemiological investigations. According to one study, using aspirin increased the chance of fracture. As a result, while aspirin may enhance bone mineral density, its effect on fracture prevention is unclear. Further research is needed to evaluate the effects of aspirin on human bone health.
Three types of bone cells from various lineages regulate skeletal tissue homeostasis. Osteoblasts, which create bones, are formed from mesenchymal stem cells that express the transcription factors runt-related factor 2 and osterix.
Osteoclasts, which oversee bone resorption, are produced from hematopoietic stem cells and exhibit specific markers such as the calcitonin receptor (CTR), tartrate-resistant acid phosphatase (TRAP), and cathepsin-K. (CTSK). Osteocytes are terminally developed osteoblasts that live in the bone matrix and can create and digest bone while also influencing the actions of other bone cells. Several intercellular signaling molecules mediate the interaction of osteoblasts and osteocytes. RANKL (receptor activator of nuclear factor kappa B) ligand (RANKL) is secreted by osteoblasts and binds to RANK on preosteoclasts, stimulating their development into osteoclasts. Osteoblasts also secrete osteoprotegerin (OPG), which acts as a decoy receptor for RANKL, limiting osteoclast development.
Several endogenous and exogenous variables regulate bone metabolism. One of the mechanisms influencing bone metabolism is prostaglandin E2 (PGE2), one of the precursors for inflammatory cytokines generated by cyclooxygenase (COX). It is required to produce osteoblasts and bone tissue and impacts osteoclast creation, by changing the RANKL-OPG axis. Prostaglandin E2 is also required for mechanical signal transduction in osteocytes.
Aspirin is the prototype agent for nonsteroidal anti-inflammatory medicines (NSAIDs), and it has antipyretic, analgesic, and anti-inflammatory properties. It inhibits all COX isoforms by creating an irreversible covalent link with the hydroxyl group of serine 530 (acetylation), preventing arachidonic acid from reaching the enzymes.
Because of the risk of gastrointestinal bleeding, aspirin is being substituted in the treatment of fever, pain, and inflammation with selective COX-2 inhibitors. Because of its antiplatelet properties, it is now more widely used at modest doses to prevent cardiovascular events in high-risk persons. Low-dose aspirin may also reduce the incidence of colorectal cancer, according to certain studies. According to data from the National Health Interview Survey (United States) in 2010, 19% of 27,157 participants aged 18 and up were regular aspirin users (at least three times a week for over three months). The number of frequent users has increased by 57% since 2005, due to its well-recognized cardiovascular system preventive benefits. Given the prevalence of aspirin use among the older population at risk of bone loss and its effects on COX, which produces PGE2, a bone metabolism regulator, the question of whether aspirin can alter bone health emerges.
The goal of this review was to outline the current evidence on aspirin’s effects on the skeletal system. Osteoporosis is a metabolic skeletal disease that primarily affects the elderly and is characterized by an imbalanced bone remodeling in which the rate of bone resorption exceeds the rate of bone production. It induces osteoporotic fracture, which is associated with considerable mortality and morbidity in patients. Because the elderly are more prone to use aspirin for disease prevention, it is critical to understand how aspirin affects their bone health.
Improving our understanding of aspirin and bone health
According to one meta-analysis of many studies, aspirin use reduced fracture risk by 17%. Nevertheless, because the studies included in the study were observational, they could only indicate a relationship between aspirin use and a lower risk of fracture. Such studies cannot prove that taking aspirin caused fewer fractures.
Further research is needed to prove or deny this idea. One, thankfully, has recently been released, and it throws into doubt whether aspirin has any effect on bone health.
The current study, which was published in JAMA, is the first to investigate a link between aspirin use and fracture risk. This study is more powerful than an observational study in determining whether aspirin use affects fracture risk.
Around 17,000 elderly people were randomly allocated to receive either a low-dose aspirin (100 mg) or an identical placebo every day. They were then monitored for fractures or major falls for five years. A serious fall was classified as one that required a trip to the emergency department or hospitalization. The average age of research participants was 74, with more than half (55%) being women and the majority being white. The researchers discovered:
- Severe falls and fractures were common, affecting 8.6% of aspirin users and 9.5% of placebo users.
- The risk of fracture did not differ between the aspirin and placebo groups.
Aspirin users had a far increased risk of major falls. This could be related to aspirin’s blood-thinning effect: an accident that would normally result in minor bruising or bleeding could necessitate medical treatment if a person were taking aspirin.
These data, in contrast to previous observational studies, do not support the use of low-dose aspirin to promote bone health or minimize fall-related fractures.
What more should you know about aspirin?
While aspirin is a safe medication, there are some drawbacks for adults to consider, including an increased likelihood of serious falls, as documented in this current study. In addition, Aspirin and other nonsteroidal anti-inflammatory medications are common causes of stomach ulcers and gastrointestinal hemorrhage.
Aspirin responses can be severe, including allergic reactions and aggravation of respiratory problems such as sinusitis or asthma.
Aspirin’s blood-thinning effect may cause significant bleeding in those with specific blood diseases (such as hemophilia) or who are currently taking another blood thinner.
For decades, aspirin treatment has been used to prevent cardiovascular disease. Recent research and guidelines, however, suggest that people should not use aspirin on a regular basis unless they have had a stroke.
Perspectives on Future Research
Many research gaps in the discipline have yet to be filled. To begin, there is no direct evidence that the previously indicated bone-protecting mechanisms of aspirin are dependent on its COX-inhibitory effects. This could be accomplished using genetically modified animals, such as COX-knockout mice.
Second, both COX-2-specific NSAIDs and aspirin are bone health protective. The efficacy of these two types of NSAIDs should be examined to determine which COX subtypes are more advantageous to bone health when inhibited.
Finally, PGE2 is required for mechanical signal transmission in osteocytes. Because aspirin can impair PGE2 synthesis, the impact of aspirin on this pathway should be investigated. Fourth, consider the negative consequences of oestrogen shortage.
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