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Diabetes and Bone Health, Arthritis Treatment FAQs

Diabetes and Bone Health and Arthritis Treatment

Diabetes or high blood sugar has adverse impact on bone health. Diabetes can certainly be complicated by bone and joint diseases, including osteoporosis and Charcot joints. Of course, non-diabetic patients can also develop osteoporosis, especially the elderly and postmenopausal women. However, due to metabolic disorders in diabetic patients, the activity of osteoclasts is enhanced. The activity of osteoblasts is weakened, and the occurrence of osteoporosis is early and severe.

Infographics on Diabetes and health of bones


 

Osteoporosis patients may not find any problems by checking blood calcium, blood phosphorus and alkaline phosphatase, but doing x-ray examination or bone density examination will find problems. 

Osteoporosis can cause bone pain and, more seriously, fractures and disability.

 

Early calcium and vitamin D supplementation is necessary to prevent osteoporosis. Charcot joints tend to occur in the feet and ankles. 

The main manifestations are skeletal deformities, especially in severe and persistent bone joints such as ankle swelling after mild trauma, and the pain is less obvious. 

This bone disease may be associated with diabetic vascular and neuropathy, but the exact mechanism is less clear. 

The treatment of Charcot joints is mainly local care, including avoiding excessive weight bearing on the affected limb or wearing special shoes to protect the affected limb, and if necessary, joint fixation surgery can be performed.

 

Diabetes and Osteoporosis

Diabetes and osteoporosis are one of the important diseases of the endocrine and metabolic system. 

The pathogenesis of each is also very complex, and the situation becomes more complicated when diabetes and osteoporosis coexist in an individual. 

Infographics on Diabetes and Osteoporosis


Below information provides a brief review of the link between diabetes and osteoporosis.

 

1. The prevalence of fragility fractures and changes in bone mineral density in diabetic patients

It is an indisputable fact that patients with diabetes have an increased risk of fractures. The prevalence of osteopenia and osteoporosis in patients with type 1 diabetes is as high as 48% - 72%. 

Do Diabetics have higher fracture risk?

Among patients with type 2 diabetes, those with poor glycemic control had a 47%-62% higher fracture risk than those without diabetes and those with good glycemic control. The risks of femoral neck and spine fractures were 2.1 times and 3.1 times higher than those of the normal population, respectively.

 

Do Diabetics have higher risk of hip fracture?

A large meta-analysis showed that patients with both type 1 and type 2 diabetes had a significantly higher risk of hip fracture than normal individuals. 

The prevalence of osteoporosis and the risk of osteoporotic fractures are thus significantly increased in the entire diabetic population compared with the general population.

 

But looking at the prevalence of osteoporosis in the diabetic population from the perspective of bone density, the situation becomes more complicated. 


Do diabetes patients have an imbalance between bone formation and bone resorption?

About two-thirds of patients with type 1 diabetes are in a state of bone turnover with a predominance of bone resorption, leading to an imbalance between bone formation and bone resorption. This explains the increased risk of fractures due to decreased bone density, which is associated with absolute insulin deficiency in type 1 diabetes and bone loss. decrease in matrix synthesis.

However, the changes of bone mineral density in patients with type 2 diabetes are still controversial. 


Do diabetes patients suffer from decrease in bone mineral density?

A large number of studies have found that the increased risk of fracture in patients with type 2 diabetes is sometimes not accompanied by a decrease in bone mineral density, and some research data even suggest that the level of bone mineral density is higher than that of normal controls. This is mainly related to the loss of bone mass in type 2 diabetes, and the factors affecting bone mass in type 2 diabetes are more complex than in type 1 diabetes, such as body mass index (BMI), insulin resistance, protein glycation, increased risk of falls and some Use of oral hypoglycemic drugs, etc.

 

Is BMD (Bone Mineral Density) of patients with type 2 diabetes significantly higher?

Further research found that although the BMD of patients with type 2 diabetes was significantly higher than that of the control group, the increase was mainly concentrated in the trabecular bone, and there was no bone change in the cortex. Therefore, some experts believe that dual-energy x-ray absorptiometry (DXA) is difficult to capture the subtle changes in bone structure and bone quality in patients with type 2 diabetes, resulting in increased fracture risk independent of bone density in patients with type 2 diabetes. This is represented by proper evaluation and monitoring.

 

Is Quality of the cortical bone in patients with type 2 diabetes impaired?

Another study found that the trabecular bone mineral density of the distal tibia and radius in diabetic patients was increased, and the porosity of the radial cortex was increased, suggesting that the quality of the cortical bone in patients with type 2 diabetes was impaired, thereby affecting the risk of diabetic fractures.

Infographic showing Bone diseases due to diabetes process


 

2. Bone turnover in diabetic patients

Bone turnover status is an important part of the pathogenesis of osteoporosis. Classification by bone turnover rate Osteoporosis is divided into three types: 

  1. High turnover
  2. Normal turnover
  3. Low turnover

For example, postmenopausal osteoporosis, hyperparathyroidism, and glucocorticoid-induced osteoporosis all belong to the high turnover type. Osteoporosis.

 

The medical definition of bone turnover refers to the bone metabolism activities of new bone formation by osteoblasts and bone resorption by osteoclasts. 

During the process of bone turnover, a variety of bone turnover biomarkers are secreted, such as osteocalcin, bone-specific alkaline Phosphatase (BAP), osteoprotegerin (OPC), type 1 procollagen amino-terminal peptide (PINP), etc. belong to bone formation indicators, while type I collagen N-terminal peptide (NTX) and type 1 collagen C-terminal peptide (CTX) belong to bone resorption index. 

The change of bone turnover index is faster than the change of bone density, which can reflect the state of bone metabolism more quickly and sensitively;

 

It has important clinical significance for the diagnosis of high-transformation osteoporosis and the monitoring of therapeutic efficacy. The bone resorption index will decrease rapidly 2-4 weeks after treatment with anti-bone resorption drugs such as alendronate, and reach 3-6 months after treatment. 

The change of bone resorption index was slightly later than that of bone resorption index, and the plateau was reached in about 6-12 months. 


What about bone turnover in diabetic patients?

Studies have shown that the level of osteocalcin in patients with type 1 diabetes decreases by nearly 4 times, and it is negatively correlated with HhA1c. 

Do diabetes patients have more bone fragility?

The type 1 diabetes patients with poor blood sugar control have more obvious bone fragility than those with ideal blood sugar control, suggesting that hyperglycemia may damage bone formation. 

Significant decreases in osteocalcin and sclerostin were also observed in patients with type 2 diabetes, and abnormalities in these biomarkers suggest that patients with both type 1 and type 2 diabetes are in a state of low bone turnover, resulting in bone mineral loss.

 

3. The possible mechanism of diabetes-induced osteoporosis

The inhibition of diabetes-induced osteoporosis is complex and not yet fully understood. In addition to gender, age, weight, race, nutritional status, etc., it is also related to bone metabolism regulators and bone mineral metabolism. 

Diabetes can affect bone metabolism through various mechanisms. It is currently believed that the following factors contribute to the development of osteoporosis in individuals with diabetes:

 

1. The effect of hyperglycemia on osteoblasts

studies have found that high concentrations of glucose (12 mmol/L or even 24 mmol/L) can alter the biomineralization process of osteoblasts and enhance mineralization, increasing RANKL, bone sialoprotein and transcription. 

Receptor Runx2 mRNA expression, reduces OPG mRNA expression, thereby reducing mineral quality. 

At the same time, due to the high osmotic pressure environment caused by high glucose, TLR-2, -3, -4 and -9 are overexpressed in osteoblasts, thereby affecting the differentiation, maturation and function regulation of osteoblasts and osteoclasts.

 

Infographics showing bones with Osteoporosis due to diabetes

The above-mentioned high-glucose environment has a series of effects on osteoblasts, which will eventually lead to a decrease in the serum osteocalcin level, which plays a key role in bone mineralization.

 

Recent studies have found that osteocalcin is an independent factor related to HbA1c, and is closely related to the aggravation of glucose metabolism disorders. Lower levels of osteocalcin in diabetic patients may reflect decreased osteoblast activity. 

Different concentrations of glucose levels have different effects on osteoblasts. Gradually increasing glucose concentration first promoted and then inhibited the proliferation of MG63 osteoblasts.

 

When the glucose concentration increased from 11.1 to 33.3mmol/L, its effect on inducing apoptosis of MC3T3-E1 osteoblasts was more obvious, and with the prolongation of culture time, the apoptosis of MC3T3-E1 osteoblasts also increased significantly. 

It can induce osteoblast apoptosis in a concentration- and time-dependent manner, suggesting that high glucose environment has toxic effects on osteoblasts.

 

High concentrations of glucose not only enhanced osteoblast apoptosis, but also inhibited their differentiation and maturation. 

Basic research suggests that glucose inhibits the differentiation of BMSCs into osteoblasts in a dose-dependent manner. 

At the same time, high glucose not only directly affects the apoptosis and differentiation of osteoblasts, but also indirectly affects the activity of osteoblasts by regulating the expression of PPARy. 

PPARy is a member of the nuclear receptor transcription factor superfamily and an important transcription factor for adipokines. 

Chronic long-term hyperglycemia increases the expression of PPAHy, which has an inhibitory effect on osteoblasts.

 

2. The effect of hyperglycemia on osteoclasts

Osteoclasts are derived from hematopoietic stem cells through the regulation and differentiation of osteoblasts through RAHKL, OPG, etc. 

Glucose as its primary energy source can stimulate osteoclasts. Studies have found that glucose concentrations of 7-25 mmol/L can maintain maximal bone resorption activity. 

It can be seen that the bone resorption of osteoclasts has a glucose concentration-dependent characteristic, and there is a rapid bone loss in the case of hyperglycemia.

 

3. Influence of insulin-like growth factor 1 (IGF-I) on bone metabolism

IGF-I can promote cell mitosis, act on osteogenic cells to stimulate DNA synthesis, promote osteoblast differentiation and enhance its activity, and regulate bone resorption at the same time, inhibits the degradation of collagen, an important growth factor secreted by skeletal cells. 

The role of IGF-I in stimulating the proliferation of osteoblast-like cells is now well established. 

Long-term hyperglycemia in diabetic patients can inhibit the synthesis and release of IGF-I, thereby attenuating the osteogenic effect of IGF-I.

 

4. Influence of insulin on bone metabolism

Insulin exerts osteogenic function through insulin receptors on the surface of bone cells, and can promote the synthesis of bone collagen tissue. 

Insulin deficiency or insulin resistance caused by diarrhoea can lead to the dysfunction of osteoblasts and the reduction of bone matrix content, and affect the synthesis of osteocalcin.

 

In type 1 diabetes, due to the absolute deficiency of insulin, the relative deficiency of insulin in type 1 diabetes affects the synthesis of collagen by osteoblasts, which can accelerate the metabolism of collagen tissue, thereby enhancing the bone resorption of osteoclasts. At the same time, the lack of insulin inhibits the synthesis of bone by osteoblasts. calcium, thereby making bone resorption greater than bone formation, ultimately leading to the formation of osteoporosis. Therefore, insulin therapy is not only beneficial to the prevention and treatment of chronic complications of diabetes, but also has positive significance in preventing osteoporosis. 

If osteoporosis is considered to be a chronic complication of diabetes, the status of insulin cannot be ignored.

 

5. The effect of advanced glycation end products (AGEs) on bones

High glucose leads to the production of a large number of AGEs in various organs and tissues, including bone matrix, and a large number of ACEs accumulate in bone tissue, causing mesenchymal stem cells to apoptosis, preventing them from differentiating into Adipose tissue, cartilage and bone, causing a marked decrease in osteogenesis. 

In diabetic patients, the glycosylation of bone proteins affects two processes of bone remodeling, namely, bone resorption by osteoclasts and bone formation by osteoblasts.

 

In addition, AGEs interact with their receptors and promote the adhesion of various inflammatory factors including interleukin (IL)-1, IL-6, TNF, intercellular adhesion molecules and vascular cells through the osteoclast and osteoblast nuclear factor pathways. 

The increased expression of molecule 1 changes the physiological function of bone collagen, promotes the maturation of osteoclast precursors, stimulates the aggregation of osteoclasts, inhibits their apoptosis, increases the activity of osteoclasts, and accelerates bone resorption, which in turn leads to disorders of bone remodeling play an important role in the development of osteoporosis.

 

6. The impact of diabetic complications on the bones

The vast majority of diabetic patients will develop diabetic vascular complications under the condition of unsatisfactory long-term glucose control, which also has adverse effects on bone metabolism. 

Hyperparathyroidism secondary to diabetic nephropathy can lead to increased bone calcium mobilization and increased bone loss. 

When combined with peripheral vascular disease, due to microcirculation disorders, the permeability of capillaries increases, and the surrounding basement membrane thickens, which affects bone reconstruction; at the same time, it affects the distribution of blood vessels in the bones, resulting in insufficient blood supply to the bone tissue, resulting in abnormal bone metabolism.

 

After diabetic cerebral infarction, the muscle strength of the affected limb decreases and the balance ability decreases, which leads to an increased risk of falling.

 

What is the effect of Hypoglycemic Drugs on Osteoporosis?

The ADOPT study found that thiazolidinediones (TZDs) were associated with increased bone loss and fracture risk in diabetic patients, especially in women with diabetes. Clinical data showed that in elderly postmenopausal women, patients taking TZDs lost bone mass at a rate of 0.61% per year compared with non-users, accompanied by a decrease in serum osteocalcin levels. 

Mice treated with rosiglitazone showed significant reductions in bone mineral density, bone mass, and changes in bone microarchitecture at 8 weeks.

Infographics showing affect of Hypoglycemic Drugs on Osteoporosis


 

These data suggest that TZDs affect bone formation in patients with type 2 diabetes. Experiments have found that TZDs can promote the occurrence and development of osteoclasts. At the same time, they can also induce the differentiation of mesenchymal stem cells into adipocytes by inhibiting the differentiation of mesenchymal stem cells into osteoblasts, which eventually leads to osteoporosis.

Diabetes Drugs on Osteoporosis


The most widely used sulfonylureas in Asia also have an effect on the bone mass of diabetic patients. UK-DPRD data show an increased risk of fracture in patients taking sulfonylureas. 

These drugs may interfere with the degradation of the phosphatase catalyst by increasing cAMP, competitively inhibit the activity of the enzyme, and increase the loss of calcium salts.

Recent domestic studies have found that sulfonylurea drugs can reduce the survival rate of MC3T3 E1 cells and increase the expression of autophagy and apoptosis marker proteins, suggesting that medium and high concentrations of sulfonylurea drugs can induce autophagy and apoptosis in osteoblasts. Decreased osteoblast differentiation function.

 

5. Treatment and Prevention

First of all, good control of blood sugar should be achieved and maintained, attention should be paid to the value and status of insulin therapy, and oral hypoglycemic drugs, such as TZDs and sulfonylureas, should be used cautiously in diabetic patients with osteoporosis risk factors to reduce or delay the complications of diabetes. disease occurrence. 

Diabetic patients without osteoporosis should pay attention to supplement calcium and vitamin D while treating diabetes to prevent the occurrence and development of osteoporosis.

 


The Impact of Diabetes on Bone Disease

A patient has been suffering from diabetes for more than 10 years, but her blood sugar can still be controlled. 

A recent physical examination revealed that she had "multiple gallbladder stones". 

The patient is puzzled, can diabetes cause stones? 

Is this a coincidence? Or are there other problems? 

In fact:

Most patients with osteoporosis have a slow onset and last for several years. 

The main clinical manifestations are backache and leg pain, finger twitching, gastrocnemius muscle spasm, bones becoming brittle and easy to break, and even deformities such as stooping of the waist, stooping, and lameness. 

X-ray examination revealed a decrease in bone density. Bone problems can lead to abnormal cartilage problems, causing osteoarthritis and affecting the ability of the elderly to exercise. 

The decline in exercise ability will also cause a decline in the ability of the body to recover, thereby affecting the overall health of the human body.

 

As we all know, diabetes mellitus is a group of metabolic diseases characterized by chronic elevated blood sugar levels. 

Osteoporosis is a metabolic bone disease characterized by low bone mass and microstructural destruction of bone tissue, leading to increased bone fragility and susceptibility to fractures. 


How can two types of diseases i.e. Diabetes Mellitus and Osteoporosis that seem to be incompatible?

We can find out the answer from the following aspects: 

1. The body of diabetic patients is continuously at high blood sugar level, which will cause the balance of calcium and phosphorus metabolism in the body to be destroyed.

 The osmotic diuretic mechanism of diabetic patients requires a large amount of glucose to be excreted, and at the same time, a large amount of mineral elements such as calcium, phosphorus, and magnesium are excreted from the body, resulting in a state of low calcium and low magnesium. 

This state will stimulate the increase of parathyroid hormone secretion, which will enhance the osteolytic effect in the human body, so the bone will be "eroded" and holes will appear, resulting in osteoporosis.

 

2. In our bones, osteoblasts are responsible for bone regeneration, or "bone building." Insulin regulates the "bone building" function of osteoblasts through insulin receptors on the surface of osteoblasts. 

Due to the absolute or relative lack of insulin in diabetic patients, the "bone building" effect of osteoblasts is weakened, so the human body is prone to osteoporosis.

 

3. Vitamin D is an important nutrient to promote calcium absorption and activation. Under normal circumstances, vitamin D needs hydroxylase in kidney tissue to "activate". However, long-term diabetes causes renal damage, the activity of this hydroxylase in renal tissue will be significantly reduced, and vitamin D cannot be fully activated. Calcium absorption is reduced due to lack of vitamin D.

 

4. A considerable number of diabetic patients are complicated by hypogonadism, and the lack of sex hormones itself will promote and aggravate osteoporosis (the process of osteoporosis in women is accelerated after menopause).

 

5. When diabetes mellitus is combined with vascular and neuropathy of bone tissue, it will aggravate the nutritional disorder of bone metabolism. 

In addition, for those patients who already suffer from primary postmenopausal osteoporosis and senile osteoporosis, having diabetes will make the condition worse.

 

Traditionally, osteoporosis is generally considered to be a natural aging phenomenon, therefore, most patients will go with the flow without active treatment. 

In fact, osteoporosis is not a simple natural physiological aging phenomenon, but is a disease that needs treatment in most cases, and there are different degrees of fracture risk.

 

According to statistics, nearly 20% of the elderly who have hip osteoporotic fractures die of various complications within one year, and more than 50% of the survivors are still disabled and unable to take care of themselves. 

According to reports, about one-half to two-thirds of diabetic patients have decreased bone mineral density, and nearly one-third of them can be diagnosed with osteoporosis. In addition, bone health has an important impact on mineral metabolism in the human body.


Osteoporosis can cause imbalance of mineral metabolism in the body, cause neurological and endocrine diseases, and also lead to cardiovascular diseases, which in turn affect the treatment of diabetes.

Therefore, it is very important for diabetic patients to actively prevent osteoporosis associated with diabetes mellitus. 

It is of great significance to improve the quality of life of diabetic patients and to save medical expenses. 

It should be highly valued by diabetic patients.

 

How to treat diabetes a simple way to lower blood sugar for better bones - very practical way. 

How to treat diabetes?

A Diabetes treatment methods include:

1. Lifestyle intervention, including diet, exercise, blood sugar monitoring, etc.

2. Drug therapy, including metformin, glyburide and other drugs

3. Surgical treatment, including insulin replacement therapy for diabetes

4. Combination therapy with insulin

5, Other drugs

6. Surgical treatment

7. Reconstruction of islet function

 

How to treat diabetes, how to treat diabetes for good bone health? Can lower blood sugar in just one week?

How to treat diabetes

A Diabetes treatment methods include:

1. Lifestyle intervention, including diet, exercise, blood sugar monitoring, etc.

2. Drug therapy, including metformin, glyburide and other drugs

3. Surgical treatment, including insulin replacement therapy for diabetes

4. Combination therapy with insulin

5. Other drugs

6. Surgical treatment

7. Reconstruction of islet function

 


Author's Bio

Doctor Shawna Reason, Virologist
Dr. Shawna Reason
Name: Shawna Reason

Education: MBBS, MD

Occupation: Medical Doctor / Virologist 

Specialization: Medical Science, Micro Biology / Virology, Natural Treatment

Experience: 15 Years as a Medical Practitioner

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