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Cannabinoid Use in Musculoskeletal Illness: a Review of the Current Evidence

The use of cannabinoids has increased since legalization of recreational and medical use in the USA. It is likely that many orthopaedic patients consume cannabinoid products during the traumatic or perioperative period. The purpose of this study was to investigate the pre-clinical data evaluating the mechanism of action of cannabidiol (CBD) and Δ 9 -Tetrahydrocannabinol (Δ 9 -THC) and to evaluate the current clinical data on the use of cannabinoids in musculoskeletal illness.

Recent Findings

Recent pre-clinical studies have demonstrated that cannabinoid use and the endocannabinoid system (ECS) has an important role in bone healing and bone homeostasis. There is data that suggests that the use of cannabidiol (CBD) may increase bone healing, whereas the use of Δ 9 -Tetrahydrocannabinol (Δ 9 -THC), the major psychoactive ingredient in marijuana, likely inhibits bone metabolism and repair. The clinical implications and consumption of marijuana by orthopaedic patients have not been thoroughly evaluated. Studies have demonstrated concern for negative cardiovascular and psychiatric effects caused by marijuana use, but have not yet elucidated outcomes in the orthopaedic literature.

Summary

With the recent increase in advertising of CBD products and legalization of marijuana, it is likely that many orthopaedic patients are consuming cannabinoid products. The clinical implications and consumption of these products are unclear. We need more robust and well-designed clinical studies prior to making further recommendations to our patients on the consumption of these products.

Introduction

Marijuana, otherwise known as Cannabis sativa, is the most commonly used illicit drug in the USA [1]. Self-reported use of cannabinoids has increased since legalization of recreational and medical use [2••, 3•]. Approximately 3.1 million individuals reported daily use in 2013 and 8.1 million reporting using marijuana most days in the last month in 2013 [4]. Data demonstrates that the number of marijuana users has steadily increased from 2002 and that in 2016 it was estimated that over 22 million Americans over the age of 12 used marijuana [2••].

Cannabidiol (CBD) is an active ingredient in marijuana, but has recently gained popularity due to extensive marketing and advertising. The Food and Drug Administration has only approved highly purified CBD for the treatment of epilepsy. However, many companies make unproven claims that CBD can treat a variety of medical maladies including acne, anxiety, opioid addiction, pain, and menstrual problems [5•]. With the increased popularity of marijuana use and advertising surrounding CBD, it is likely that many orthopaedic patients consume cannabinoid products during the perioperative period [5•, 6•].

It is known that cannabinoids have a number of effects on the body and specifically on the musculoskeletal system. There is a growing body of literature on cannabinoid use, its biomechanical impacts on the musculoskeletal system and on the effect of cannabinoids in orthopaedic surgical outcomes. The primary purpose of this review is to critically analyze the current data on cannabinoid mechanism of action on the musculoskeletal system and its use in the treatment of musculoskeletal illness.

The Endocannabinoid System Positively Affects Bone Mass and Cellular Differentiation

The endocannabinoid system (ECS) is comprised of two G protein–coupled receptors: CB1 and CB2, activation of which inhibit adenylyl cyclase activity. Current research suggests that both receptors serve a common role in the modulation of chemical messengers from various cell types [7]. High concentrations of CB1 receptors have been identified on neurons and CB2 receptors on immune cells, suggesting their role in both neuro- and immunomodulation. Furthermore, the CB1 and CB2 receptors and their associated endogenous cannabinoid ligands have been shown to be cytoprotective in many cell types [8, 9].

CB1 and CB2 receptors are associated with endogenous ligands, termed endocannabinoids. These are eicosanoids, derived from fatty acids, and include anandamide and 2-arachidonoylglycerol and their degradative enzymes fatty acid amide hydrolase and monoacylglycerol lipase [7, 10]. The endocannabinoids along with their corresponding receptors make up the endocannabinoid system (ECS).

Recent studies suggest that the ECS affects regulation of bone mass maintenance through CB1 and CB2 receptor activity. Another G protein–coupled receptor, GPR55, is activated by certain endocannabinoids and antagonized by CBD, and appears to inhibit CB1 and CB2 receptor activity. Inactivation of the GPR55 receptor in male mice produces phenotypes with increased bone mass and increased bone resorption [11]. The complete physiologic function of the GPR55 receptor at this time is yet largely unknown [12, 13].

CB1 receptor activity appears to serve a protective role in regulating bone mass and osteoporosis through adipocyte and osteoblast differentiation, as well as expression of multiple intracellular signaling proteins [14]. CB1 deactivation in knockout mice has demonstrated short-term in vivo increased bone mass with ovariectomy-induced bone loss [15]. Further investigations have shown age-related osteoporosis at 12 months in CB1 knockout mice. It is believed the increased bone mass at 3 months is secondary to reduced osteoclast activity and at 12 months, the osteoporotic changes are the result of defects in osteoblast differentiations and the accumulation of adipocytes in the bone marrow [13, 16]. Cannabinoid receptor deficiency in mouse models is confounded by the fact that the effects of cannabinoid receptor deficiency are age and sex dependent [13].

CB2 receptor function also appears to affect bone mass maintenance, first through direct stimulation of osteoblasts and stromal cells, and second through inhibition of RANKL expression [17]. CB2-deficient mice have a low bone mass phenotype, similar to CB1 knockout mice at 12 months. Conversely, activation of the CB2 receptor has been shown to increase bone mass by increasing the number and activity of osteoblasts, inhibiting osteoclast proliferation and stimulating fibroblastic colony formation by bone marrow cells [17–19].

The ECS also appears to affect mesenchymal stem cell (MSC) differentiation through cannabinoid receptors on mesenchymal stem cells [16, 17, 20]. Research has demonstrated a functional increase in the CB1 receptor during osteogenesis. Based on an in vivo model, it is likely that the CB1 receptor also has a functional role in the survival of the differentiated MSCs [7].

ESC activation may enhance not only MSC survival but also migration and chondrogenic differentiation of MSCs. Among other benefits, this has potential for use in mesenchymal stem cell–based tissue-engineered cartilage repair strategies; however, data on the role of the cannabinoid system in cartilage tissue is currently lacking [21].

Δ 9 -THC Activates CB1 and CB2 but Has Cytotoxic Properties

The Cannabis sativa plant otherwise known as marijuana contains more than 100 cannabinoids; the major constituents are Δ 9 -Tetrahydrocannabinol (Δ 9 -THC) and cannabidiol (CBD) [10, 20]. The psychoactive ingredient in cannabis is Δ 9 -THC and although it also has analgesic and anti-emetic effects, it is best known for its psychoactive effects [10, 22].

Δ 9 -THC is a partial agonist of the CB1 and CB2 receptors, but has higher affinity for the CB1 receptor. The effects of Δ 9 -THC are largely due to the activation of CB1 receptors in the nervous system affecting control of synaptic activity, motor function, pain perception, and appetite [23]. This nervous system activation gives rise to marijuana’s euphoric effects, but carries the frequent side effect of memory impairments and an increased risk of psychosis [23].

Despite its activation of CB1 receptors, Δ 9 -THC may have a detrimental effect on bone healing. Δ 9 -THC has a dual toxicity profile that prevents osteogenesis and induces cell death in a number of cell types, including neurons and mesenchymal stem cells, likely via a proapoptotic downstream signaling mitochondrial pathway [7]. For this reason, Δ 9 -THC is being investigated for possible use as an anti-tumoral agent [7, 23–26].

Cannabis smoke inhalation, similar to tobacco smoke, has been shown to reduce bone healing around titanium implants in a rat fracture model [27]. This raises concerns for implant survival and bone healing in patients after fracture fixation. In particular, the impact of Δ 9 -THC on mesenchymal stem cell differentiation suggests a negative effect on osteogenic potential and resultant bone healing [7].

The effects of marijuana on bone homeostasis and fracture healing are under current investigation. Heavy cannabis use has been linked to low bone mineral density, low BMI, high bone turnover, and increased risk of fracture [13]. It is currently unclear to what extent this is caused solely by the ingestion of Δ 9 -THC.

Cannabidiol Antagonizes GPR55 Thereby Facilitating CB1 and CB2

Cannabidiol (CBD) is another popular cannabinoid of the Cannabis sativa plant. CBD has no psychoactivity and is primarily an anti-inflammatory [1, 28]. CBD has been well studied for a number of illnesses including neurodegenerative disease, epilepsy, and immune disorders such as multiple sclerosis, arthritis, and cancer [29•]. Currently, it is FDA approved only for the treatment of epilepsy [29•].

CBD antagonizes cannabinoid receptor GPR55, and is thus an inverse agonist of the CB2 receptor. Compared with Δ 9 -THC, CBD has lower affinity to the CB1 and CB1 receptors. In vivo studies have demonstrated that CBD can inhibit bone resorption via modulation of GPR55 signaling and activation of CB2 receptors. It is unknown whether Δ 9 -THC acts on the GPR55 receptor, and if so, whether it has similar or opposing effects to CBD.

The effect of CBD in fracture healing has been investigated in a rat model evaluating callus formation about femur fractures. This data demonstrated enhanced biomechanical properties of healing rat mid-femoral fractures in rats given CBD compared with a control group. This effect was not shared by rats given only Δ 9 -THC; moreover, attenuation of the osteogenic CBD effect was seen in rats given equal amounts of CBD and Δ 9 -THC. This favorable biological effect of CBD is believed to occur via enhancement of osteoblastic expression of lysyl hydroxylase 1, a collagen crosslinking enzyme [28]. Similar in vivo research has shown that CBD incorporated into an osteoconductive scaffold can stimulate MSC migration and osteogenic differentiation [28]. Further studies are needed to better evaluate the role of CBD in human bone healing and metabolism, as well as the long-term effects of CBD ingestion [30•].

Minimal Evidence Regarding Orthopaedic Surgical Outcomes in Marijuana Users

While recent pre-clinical data has demonstrated promising effects of CBD on bone healing and bone metabolism, clinical studies are insufficient and inconclusive. A retrospective review of the National Hospital Discharge Survey (NHDS) evaluated patients who underwent primary total joint arthroplasty and found that patients who abused substances preoperatively had higher rates of surgery-related complications. Significantly, this study was not limited to marijuana users and included patients using opioids, cocaine, cannabis, amphetamines, inhalants, and sedatives [31].

Research surrounding marijuana in the total joint arthroplasty cohort is contradictory. In a recent series, Law et al. performed a retrospective review of the Medicare database on total knee arthroplasty (TKA) patients evaluating those who used marijuana compared with those who did not. This study found a significant increase in reoperation rate due to infection in the cohort that used marijuana. This study was limited as they relied on accurate coding for data collection and further did not stratify patients based on additional risk factors [32••].

In comparison, a recent retrospective cohort study using a matched control and selected patients only using marijuana versus other substances found no difference in complications after primary TKA in patients that did and did not use marijuana [3•]. The limitations of this study must be appreciated as well, as not all patients report use of substances, and frequency and type of use may not be properly recorded [3•].

A recent review analyzed data from the Healthcare Cost and Utilization Project Nationwide Inpatient Sample (HCUP-NIS) database to evaluate the effect of marijuana use by orthopaedic patients on inpatient mortality, heart failure, stroke, and cardiac disease. A decreased mortality rate was seen in patients who used marijuana compared with those who did not [2••]. Similar to previous studies, this study did not stratify by comorbidities, nor by demographics of marijuana users. Furthermore, the heart failure, stroke, and cardiac disease codes generated during hospital visits were likely in part preexisting conditions rather than complications of hospitalization.

Marijuana use does not only affect the musculoskeletal system, nor is marijuana ingestion limited to CBD and Δ 9 -THC. The smoke from cannabis has been shown to contain many of the same carcinogens as tobacco, and heavy cannabis use has been associated with an increased risk of developing lung cancer [1]. Patients using marijuana are at increased risk of psychiatric effects including anxiety, agitation, and even acute psychosis [33]. Other studies report potential increased risk of cardiac events, atherosclerosis, and even stroke in patients that smoke marijuana [34–38].

The current conflicting data on marijuana use in an orthopaedic surgical population demonstrates the need for future well-designed prospective studies evaluating outcomes and potential complications. It is possible that the perioperative use of marijuana or CBD alone may significantly impact healing, recovery, and complication rates after orthopaedic procedures.

Cannabinoid Use for Musculoskeletal Pain

Opioid over-consumption among patients with musculoskeletal pain is of top concern to orthopaedic surgeons given recent trends in morbidity and mortality associated with chronic narcotic use [3•]. Accordingly, alternatives to narcotic use have recently gained substantial attention. Many patients with complicated surgical history, large-scale procedures, or multiple comorbidities require multimodal pain medication regimens [3•]. Cannabinoids, if effective for pain relief, could potentially reduce the opioid burden [3•, 39•].

Pre-clinical studies demonstrate that cannabinoid signaling has an integral role in the nociceptive system and that CB1 and CB2 receptor agonists have antinociceptive properties. Δ 9 -THC has also been shown to have euphoric and psychoactive effects, both of which have a role in pain modulation and experience [7]. Clinical evidence has not demonstrated similar findings in human experiments [40•]. No clear benefit from the use of cannabinoids has been shown to be better than placebo [41•]. This result is due in part to a lack of high-quality evidence to support the use of medical marijuana therapy for acute or chronic pain indications [41•]. The paucity of high-quality data is not only an issue in musculoskeletal pain, but is part of the larger lack of evidence supporting the common use of marijuana for chronic rheumatologic, oncologic, or arthritic pain [33, 39•,41•].

Conclusion

Pre-clinical studies demonstrate that the ECS has an important role in bone healing and bone homeostasis. There is promising evidence that CBD may increase bone healing through activating cannabinoid receptors, whereas Δ 9 -THC likely inhibits bone metabolism and repair. Current mouse and rat models are age and sex dependent, limiting generalizability and applicability to human cannabinoid receptor function [13]. It is currently unclear whether the pre-clinical evidence demonstrated in this review will correlate with clinical evidence in bone formation and homeostasis in humans.

The perioperative consumption of marijuana by orthopaedic patients has more relevant factors to consider than only the ingestion of specific cannabinoids. Marijuana smoke contains carcinogens similar to tobacco smoke, and has not been thoroughly evaluated as a cause of perioperative or long-term complications. Studies have demonstrated concern for negative cardiovascular and psychiatric effects caused by marijuana use, but have not elucidated similar orthopaedic complications. Future areas for research include age- and comorbidity-stratified analysis of clinical outcomes in marijuana users to non-users. The consumption of CBD alone or in combination with Δ 9 -THC as conventional marijuana may have significant clinical effects in the realm of bone metabolism and fracture healing.

Compliance with Ethical Standards

The study has been performed in accordance with the ethical standards in the 1964 Declaration of Helsinki and has been carried out in accordance with relevant regulations of the US Health Insurance Portability and Accountability Act (HIPAA).

This work was performed at The Albany Medical Center, Albany, NY.

Casey M. O’Connor, Afshin A. Anoushiravani, Curtis Adams, Joe Young, Kyle Richardson, and Andrew J. Rosenbaum declare that they have no conflicts of interest.

This article does not contain any studies with human or animal subjects. Informed consent was not required for this study as it did not study human subjects.

Footnotes

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

CBD for Osteoporosis: Can Hemp Oil Help Reverse Bone Loss?

Exciting new research has been exploring CBD’s powerful ability to speed fracture healing and preserve bone density.

Learn how it works and how to use CBD products for osteoporosis effectively.

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Estimates suggest more than 200 million people have osteoporosis around the world [1].

According to the International Osteoporosis Foundation, osteoporosis is responsible for a staggering 8.9 million bone fractures annually — meaning there’s an osteoporotic fracture roughly every three seconds [2].

Often referred to as a “silent disease,” many people don’t realize they have the condition until a fracture occurs.

Here, we will discuss osteoporosis, current treatment options, and scientific research on how CBD can help.

MEDICALLY REVIEWED BY

Updated on June 05, 2021

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How Does CBD Help With Osteoporosis?

CBD (cannabidiol) is the primary non-psychoactive compound in cannabis. It’s been shown to support bone metabolism indirectly through its effects on the endocannabinoid system (ECS).

The ECS is a complex network of receptors that work to regulate various aspects of our health — including the formation and degeneration of bone [3]. Through this system, CBD is thought to help reduce bone loss and promote the regeneration of lost bone tissue.

CBD should always be used in combination with other therapies for maximum benefit. CBD is not a cure for osteoporosis, but can offer a powerful supportive role when used alongside other medications, supplements, and exercises.

The benefits of CBD oil for osteoporosis may include:

  • May improve the density of bones
  • Alleviates pain & inflammation
  • Supports hormone balance
  • Relieves pain from bone fractures

1. CBD May Improve Bone Density

Research has discovered that CBD appears to enhance the growth and strengthening of bones through accelerated osteoblast formation.

Researchers believe that osteoclasts — the cells that breakdown bone — have a cell receptor that, when activated, speeds up bone loss and degeneration. This receptor is known as GPR55. CBD has been shown to specifically block the activation of this receptor, reducing osteoclast activity [5].

Further, in a recent study in Israel, mice were given CBD or a combination of THC and CBD. The study found that the administration of CBD alone has significant effects on fracture healing with increased bone strength and toughness by stimulating Lysyl Hydroxylase — an enzyme involved in bone healing [5].

This research has given us a deeper insight into how CBD influences the body and opens up some exciting potential for further research.

2. CBD Alleviates Pain & Inflammation

CBD may have a therapeutic role in inflammation and healing. It has long been used by people with chronic pain and offers a non-habit-forming alternative to pain medications.

Many patients have reported replacing their prescription pain medications with CBD, with evidence that its use can help in the treatment of headaches, mental health disorders, insomnia, arthritis, and other chronic pain syndromes [6].

What’s The Dose of CBD Oil For Osteoporosis?

The key is to start low and go slow.

As yet, there are no standardized dosing guidelines for CBD use. CBD oil can come in many different strengths. As products vary greatly, it’s important to read the label of the specific product you are using.

When it comes to managing osteoporosis, the benefits will take several months before any change is noticed. We recommend starting with a moderate dosage (based on your weight using our CBD oil calculator below).

If you experience side-effects (more on this later), reduce the dose until they disappear.

CBD Oil Dosage Calculator

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Is CBD Oil Safe?

CBD is safe, even at high doses — but there are a few exceptions to be aware of.

According to the WHO, CBD oil, in its pure state, does not cause harm or have the potential for abuse — even at high doses [7].

If you’re using any prescription medications, or have underlying health issues, you should always speak with your doctor before taking CBD. Certain medications may interact with CBD and lead to side-effects.

What is Osteoporosis?

Osteoporosis means “porous bones.” It results in fragile bones. The weakness of the bones puts those affected at a higher risk of fractures.

As the bones become thinner, even a minor fall or bump can cause a serious injury.

Middle-aged women are at the highest risk — however, men are also affected.

The main concern most people have when talking about osteoporosis is the high risk of bone fracture. A fracture is a complete or partial break in a bone.

It’s estimated that 50% of women and 20% of men over the age of 50 will have an osteoporosis-related fracture in their lifetime [1].

With osteoporosis, the most common bones affected are the hip, wrists, and spine. Fractures and breaks can lead to chronic pain and mobility issues.

Understanding the Definitions
  1. Cortical bone — the hard outside layer of all bones and makes up most of your skull and ribs.
  2. Spongy bone — occurs inside the vertebrae and the ends of the long bones, such as the thigh bones.
  3. Osteoblasts — specialized cells involved in producing new bones.
  4. Osteoclasts — specialized cells involved in breaking down bones.
  5. Bone density — the amount of mineral content in a bone.

Symptoms of Osteoporosis

There are no specific symptoms of osteoporosis — the first sign is usually a bone fracture. There are other symptoms, but these can be difficult to identify.

Other signs and symptoms may include:

  • Back pain
  • Collapsed or fractured vertebra
  • Loss of height
  • Stooped posture
  • Lowered grip strength

Menopause & Osteoporosis

In osteoporosis, there is a thinning of the cortical bone and reduced bone density and structure in the spongy bone. Menopause is one of the main causes of the condition.

Bone tissue is continuously broken down and replenished. It’s a regular cycle, fluctuating on both a daily and monthly basis — affected by things such as time of day, diet, and season.

Specialist cells within the bones called osteoblasts and osteoclasts are essential for these fluctuations in healthy bones. From birth to adolescence, more bone is formed than broken down.

By the end of adolescence, bone growth has completed. By your mid to late 20s, peak bone mass has been achieved.

The sex hormones estrogen and testosterone have a major role in maintaining healthy bones in both men and women.

In menopause, as estrogen levels drop, the balance of hormones that were working to control bone density begins to fall apart. The result is an acceleration in bone loss. Women can lose up to 10% of their total bone mass within the first five years of menopause.

Risk Factors for Osteoporosis

  1. A family history of osteoporosis
  2. Previous bone fractures
  3. Age — people over 50 are at the highest risk
  4. Early menopause — before the age of 45
  5. Weight — being overweight is a major risk factor
  6. Vitamin D — important in the maintenance of bone tissue
  7. Calcium intake — calcium is a key mineral in bone architecture
  8. Lack of exercise — weight-bearing exercises directly lower the risk of osteoporosis
  9. Smoking (linked with osteoporosis)
  10. Alcohol intake — over three standard drinks per day increases the risk of osteoporosis [1]
  11. Medications — such as corticosteroid use
  12. Medical conditions — such as thyroid problems, celiac disease, chronic liver disease, kidney disease, or rheumatoid arthritis
  13. Conditions that affect the absorption of nutrients — such as Crohn’s disease, celiac disease, and other inflammatory bowel conditions

Diagnosing Osteoporosis

If osteoporosis is suspected, your doctor will most likely send you for a bone density scan.

This scan is used to measure bone mineral density (BMD). It is usually performed using a dual-energy x-ray absorptiometry (DEXA). This is a non-invasive process where, for 10 to 15 minutes, a machine passes over your body while you lie flat on a table.

The bone density scan will give you a T-Score and Z-Score, used to determine your risk of developing a fracture and whether further tests are needed.

According to the World Health Organization (WHO), your T-Score is classed as follows:

  • -1.0 or above is normal bone density.
  • Between -1.0 and -2.5 means you have low bone density or osteopenia.
  • -2.5 or below is a diagnosis of osteoporosis.

The following procedures can also be performed to determine bone injury or fractures as a result of osteoporosis:

1. Bone X-Ray

Bone x-rays produce images of bones that aid in the diagnosis of fractured bones, which are sometimes a result of osteoporosis.

2. CT Scan

CT scans of the spine are used to assess alignment and fractures. They can be used to measure bone density and determine whether vertebral fractures are likely to occur.

3. Magnetic Resonance Imaging (MRI)

An MRI of the spine is used to evaluate vertebral fractures for evidence of underlying diseases, such as cancer, and to assess the newness of the fracture.

How is Osteoporosis Treated?

Depending on how severe your osteoporosis is and your risk of bone fracture, your doctor may recommend lifestyle changes to strengthen your bones.

Lifestyle changes can help to ensure both men and women take steps to prevent the risk of developing osteoporosis.

1. Lifestyle & Diet Changes
  1. Incorporate a varied diet with plenty of fresh fruit, vegetables, and whole grains
  2. Avoid smoking
  3. Reducing alcohol intake
  4. Limit caffeine
  5. Do regular weight-bearing and strength-training activities
  6. Ensure adequate vitamin D and calcium intake

However, if your osteoporosis is more advanced, lifestyle changes alone may not be enough to help you strengthen your bones.

Prescription medications are standard care in the treatment of established osteoporosis. Their purpose is to either increase the formation of new bone or slow down the breakdown process.

However, they each come with their own set of side-effects and risks.

2. Bisphosphonate Medications

Bisphosphonates encourage bone density by slowing the breakdown of cells. You can take them with a combination of vitamin D and calcium supplements.

Side-Effects of Bisphosphonates:

  • Flu-like reactions
  • Stomach upsets
  • Diarrhea and constipation
  • Joint and muscle pain
  • Fatigue
  • Jaw pain
  • Jaw infection(rare)
3. Selective Estrogen Receptor Modulators (SERMs)

SERMs mimic estrogen in the body, reducing bone loss and increasing bone formation.

Side-Effects of SERMs:

  • Hot flushes
  • Leg cramps
  • Increased risk of blood clots and fatal stroke
4. Denosumab

This is given via an injection under the skin twice a year. It slows down the breakdown of bone, resulting in higher bone mineral density and reduced fractures. It is often used as an alternative to bisphosphonates.

Side-Effects of Denosumab:

  • Joint and muscle pain
  • Eczema
  • High cholesterol
5. Hormone Replacement Therapy (HRT)

Doctors prescribe HRT for women during menopause when there is a drop in estrogen levels, increasing the risk of osteoporosis. However, HRT is no longer routinely recommended due to the increased risks with long-term use.

Side-Effects of HRT:

  • Breast cancer
  • Heart attack
  • Stroke
  • Blood clots
6. Testosterone Therapy

When testosterone levels are low in men, doses of testosterone are given by injection to improve bone density.

Side-Effects of Testosterone Therapy:

  • Acne and oily skin
  • Worsening of sleep apnea
  • Increased risk of blood clots
  • Increased risk of prostate abnormalities
  • Enlarged breasts in men
  • Decreased testicular tissue
  • Increased aggression, mood swings
  • Increased risk of heart disease and stroke (maybe)

Final Verdict: Using CBD for Osteoporosis

Osteoporosis can be a debilitating disease, and the fear of bone fracture can have a significant effect on one’s lifestyle and mobility.

While there is no cure, there is good evidence that CBD may be an effective treatment for osteoporosis by slowing down the progression of the disease and relieving pain.

These are very exciting times, especially as we look at CBD and the clinical research that’s still in its infancy regarding verifying its use in reducing bone loss and fracture.

Based on this information, CBD is seen as a safe, effective, all-natural therapeutic treatment for osteoporosis.