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Osteoporosis and diabetes are two very common endocrinological diseases, affecting a large percentage of our fellow human beings.
People with type 1 diabetes mellitus present overall decreased bone density compared to people of the same age without diabetes, as well sixdouble the risk of hip fractures. Therefore, type 1 diabetes mellitus is considered an independent risk factor for fractures and for this very reason it has been incorporated into the FRAX model.
Many mechanisms have been proposed to explain this pathophysiological connection, the main one being the disruption of the normal cycle of bone regeneration (boneremodeling). Normally, there is a relative balance between bone resorption and the production of new bone tissue. In people with type 1 diabetes, the balance is disturbed and bone resorption exceeds production, resulting in low bone density. This is probably due to decreased concentrations of insulin and growth factor IGF-1, leading to reduced osteoblastic activity. Another important factor contributing to the reduction of bone remodeling is the accumulation of advanced glycation end products (AGEs) in collagen, as a result of hyperglycemia.
About him type 2 diabetes mellitusthe evidence for low BMD and increased fracture risk exists but is less clear compared to type 1 diabetes. In a meta-analysis of studies, the relative risk of hip fracture in people with type 2 diabetes was found to be 2.8 times higher in men and 2.1 times higher in women; with no significant differences for increased risk of fractures in other areas of the body.
Bone mineral density measurement is the most useful tool for estimating fracture risk in the general population. In patients with type 2 diabetes, however, it seems that it is not so reliable, since it has been found to be reduced, normal, and even increased in different studies compared to people without diabetes. This observation raises the question of the reduced quality of bones due to their disturbed microarchitecture, which is not always reflected in the measurement of bone mineral density. This is mainly attributed to accumulation of advanced glycation end products (AGEs) as a result of hyperglycemia.
Other negative contributing factors are attendance kidney diseasethe vitamin D deficiencypossible co-occurrence hypogonadism and the systemic low-grade inflammation, which cumulatively reduce the quality and strength of the bones. Complications of diabetes mellitus such as retinopathy and vision loss as well as peripheral neuropathy also increase the risk of falls and therefore the possibility of fractures.
Healthy dietary treatment with a change in eating habits and the inclusion of exercise in daily life are the cornerstone in the management of patients with type 2 diabetes, alongside medication. Many pharmaceutical agents are available, with different effects on bone metabolism and fracture risk. Metformin, sulfonylureas, thiazolidinediones, DPP-4i, GLP1-RA, SGLT-2i, and insulin are the most commonly used drugs.
THE insulin is the treatment of choice for people with type 1 diabetes, due to autoimmune destruction of pancreatic β cells and a deficiency of endogenous insulin production. Experimental studies as well as data from observational studies indicate its protective role metformin in bone health. The majority of studies demonstrate a beneficial or at least neutral effect on bone metabolism and fracture risk and for sulfonylureas. However, the high risk of hypoglycemic episodes, which may increase the incidence of falls and thus fractures in these patients, must be considered. Within a few years of the start of circulation and use of of thiazolidinediones for the treatment of type 2 diabetes there was evidence of a negative effect on bone density and an increased risk of fractures. This negative effect was later confirmed in randomized clinical trials and meta-analyses of studies.
About them DPP-4i there is more evidence of a neutral or even possible beneficial effect on bone health. The results of the effects of GLP1-RAs on bone metabolism appear positive, but must be interpreted with caution and bearing in mind that the trials that demonstrated them were not designed to study these parameters. The SGLT-2i class has several drugs. Regarding bone health, canagliflozin has been shown to have negative effects on both bone density and fracture risk, particularly of the hip. THE empagliflozin and the dapagliflozin have not shown significant changes in bone mineral density, bone markers, or fracture risk, but concerns arising from studies with canagliflozin affect the entire class of these drugs.
It has been shown that patients treated with insulin generally have an increased incidence of fractures. The chronicity of the disease, the more frequent presence of diabetic complications, the increased risk of falling due to both the above and the hypoglycemic episodes due to insulin treatment, may contribute to the increase in fracture risk and ultimately not the insulin itself, an otherwise anabolic hormone, affecting bone quality.
Maintaining a normal body weight, a Mediterranean diet rich in unsaturated, omega-3 fatty acids and nuts, adequate intake of calcium and vitamin D with careful consumption of fatty dairy products, limited intake of alcohol and salt are interventions that simultaneously promote proper glycemic regulation and bone health. Brisk walking to say the least 150 minutes per week could ideally combine the aerobic type of moderate intensity exercise indicated for diabetes mellitus and the exercise indicated for the prevention and treatment of osteoporosis. Smoking cessation is particularly important for both conditions and should be emphasized.
Metformin, DPP-4i and GLP1-RAs should be preferred in patients with type 2 diabetes who also have osteoporosis. Pioglitazone and canagliflozin should be avoided, while the other SGLT-2i are less reliable options for these individuals. Insulin should be used with caution to avoid hypoglycaemia, and this of course also applies to people with type 1 diabetes. Strict glycemic control targets should be avoided on a case-by-case basis for fear of hypoglycaemia, falls and subsequent fractures. . In addition, most patients with diabetes have hypertension, so proper control with careful avoidance of hypertensive and hypotensive episodes is particularly important. Additionally, normal vision of these individuals with at least an annual fundoscopy examination, as well as evaluation for the presence of possible neuropathy, are also important measures to prevent falls and subsequent fractures.
According to the current guidelinespeople with type 1 diabetes should have their bone mineral density checked before the age of 50 and certainly when they show any fracture. For people with type 2 diabetes, the same applies as for the general population, i.e. bone density measurement at 65 years or after 50 if other factors are present, such as a fracture in the same person or a hip fracture in the parent, alcohol consumption and smoking. If a patient with diabetes mellitus is diagnosed with osteoporosis, they should be treated appropriately with medication.
Regarding the possible effect of anti-osteoporotic drugs on glucose metabolism, the data so far show a possible improvement of glycemic control with the use of bisphosphonates, but further investigation of the subject with well-designed studies is needed. Furthermore, the effectiveness of anti-osteoporotic treatment does not seem to differ in people with diabetes mellitus. Thus, both treatment and monitoring of osteoporosis should be carried out as indicated by international guidelines and without special modifications due to the presence of diabetes.
The article comes from Mrs. Pashou’s speech at the 2023 Panhellenic Conference of the Hellenic Society for the Study of Bone Metabolism (EEMMO), 2023.