User:Bgentry12/Monckeberg's arteriosclerosis

Mönckeberg's arteriosclerosis, or Mönckeberg's sclerosis, is a form of arteriosclerosis or vessel hardening, where calcium deposits are found in the muscular middle layer of the walls of arteries (the tunica media). It is an example of dystrophic calcification. This condition occurs as an age-related degenerative process. However, it can occur in pseudoxanthoma elasticum and idiopathic arterial calcification of infancy as a pathological condition, as well. Its clinical significance and cause are not well understood and its relationship to atherosclerosis and other forms of vascular calcification are the subject of disagreement. Mönckeberg's arteriosclerosis is named after Johann Georg Mönckeberg, who first described it in 1903.

The severity of calcium deposits formed by Mönckeberg's arteriosclerosis can be categorized into stages based on the histological appearance. Understanding these stages can help to understand disease progression and how the disease is caused. Stage 1 involves the formation of calcium deposits both inside and outside the vascular smooth muscle cells which compose the tunica media. Calcification outside of the vascular smooth muscle cells are commonly associated with damage to elastic fibers in the extra-cellular matrix. These calcium deposits also develop on the internal elastic lamina. Stage 2 and Stage 3 involve the formation of calcified sheaths spanning an increased diameter through the tunica media. Stage 4 then involves the formation of bony tissue from these calcifications through the process of osseous metaplasia.^[1][2]

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Typically, Mönckeberg's arteriosclerosis is not associated with symptoms unless complicated by atherosclerosis, calciphylaxis, or accompanied by some other disease. However, the presence of Mönckeberg's arteriosclerosis is associated with poorer prognosis. This is probably due to vascular calcification causing increased arterial stiffness, increased pulse pressure and resulting in exaggerated damage to the heart and kidneys. The clinical symptoms of Monckeberg's arteriosclerosis are similar to giant cell arteritis (GCA) and which can be mistakenly interchanged. A temporal artery biopsy (TAB) can be performed to differentiate between the two disease states.^[3]

Mönckeberg's arteriosclerosis has little or no impact on the risk of microvascular surgery.^[4] Mönckeberg's arteriosclerosis is typically an incidental finding, detected through clinical examination or plain radiography, and may be associated with diabetes mellitus or chronic kidney disease. The condition is characterized by calcification of the tunica media, leading to hardened, pulseless vessels that often still provide normal distal perfusion, unlike atherosclerosis where the tunica intima is affected and the vessel lumen diameter is compromised. Despite its prevalence being less than 1% of the population, Mönckeberg’s arteriosclerosis generally does not adversely affect the outcome of microvascular surgery, as evidenced by successful free flap reconstructions using these vessels with minimal impact on flap survival.^[4]

A 75 year old South Asian male presents with complaints of an unilateral headache and overall head and facial pain, with specific pain centered on the left side of their neck. The individual had first noticed the pain about two weeks before their visit to the clinic. The pain was described to be ongoing and continuous throughout the day and rated 6-7 on the numerical visual analog scale (VAS). They reported no relieving factors and multiple associated factors including scalp tenderness and non-specific shoulder pain. The individual had tried multiple pain medications medications ranging from over the counter medications (OTC) to prescription medications including pregabalin and indomethacin but had reported to receive no pain relief from any of the medications they had taken. An orofacial pain evaluation was performed which resulted in no abnormalities found in the patient. The individual had their pain, which was produced by Mönckeberg medial arteriosclerosis, controlled by using high dosed corticosteroids combined with the usage of warm compresses and transcutaneous electrical nerve stimulation (TENS).^[5]

A 28 year old male in Saudi Arabia presented with swelling in both of his thighs, despite no past medical history significant of chronic illness, trauma, or surgeries. The individual noted significant pain due to the swelling and reported difficulty walking. As a result of this, the individual was subjected to physical examination, hematological investigations, and a variety of imaging such as a doppler examination, radiograph and MRI. This testing uncovered calcified arteries and a collection of soft tissue near the femoral arteries and veins, which lead to a disruption in the right femoral artery. Extensive analysis of the individual's condition lead medical professionals to the conclusion that Mönckeberg's arteriosclerosis was suspected as the cause for their symptoms. The individual was treated with antibiotics, bed rest, ice packs, as well as anticoagulation therapy. They also received an interventional surgery to help remove the excess fluid from their thighs. After subsequent follow-up, the individual's ability to walk was restored and imaging of their arterial calcification had improved.^[6]

A 59-year-old male patient showed up at his dental clinic for poor denture stability and was found with Monckeberg arteriosclerosis following the tomographic examination. He has a notable medical history of type 2 diabetes, hypertension, and a kidney transplant. The cone-beam computed tomography (CBCT) scan conducted before overdenture implantation detected multiple vascular calcifications in the soft tissues of both the upper neck and cheeks. These calcifications formed a tubular or “tram-track” shape, which was highly suggestive of Monckeberg arteriosclerosis.

A case report describes a 69-year-old female with Monckeberg’s arteriosclerosis affecting her uterine vessels, following long-term endometritis and experiencing premature menopause. ^[7]

Mönckeberg medial arteriosclerosis, also known as medial arterial calcinosis, is a condition where the tunica media layer of blood vessels calcifies, visible on plain radiography or sectional tomography, and can sometimes be detected in dental panoramic radiographs. Unlike atherosclerosis, which affects the tunica intima and alters the vessel lumen, this condition is associated with diabetes mellitus or chronic kidney disease, and dental treatment is safe when the patient's diabetes is well-managed.^[8]

Diagnosis of this rare disease is often misdiagnosed or delayed, leading to results such as amputation and death. Due to this, it is important to utilize comprehensive medical testing, examination, and diagnostic tests.^[9]

Often Mönckeberg's arteriosclerosis is discovered as an incidental finding in an X-ray radiograph, on mammograms, in autopsy, or in association with investigation of some other disease, such as diabetes mellitus or chronic kidney disease. The diagnosis is usually confirmed by a radiography result or an ultrasonography.^[10] Typically calcification is observed in the arteries of the upper and lower limb although it has been seen in numerous other medium size arteries. In the radial or ulnar arteries it can cause "pipestem" arteries, which present as a bounding pulse at the end of the calcific zone. It may also result in "pulselessness." Epidemiological studies have used the ratio of ankle to brachial blood pressure (ankle brachial pressure index, ABPI or ABI) as an indicator of arterial calcification with ABPI >1.3 to >1.5 being used as a diagnostic criterion depending on the study. However this type of non-invasive diagnostic tool could lead to falsely elevated values, especially individuals with diabetes that have lower limb ischemia. In an observational study, 11% of patients that met the criteria of diabetes and critical ischemia had exhibited false ABI levels.^[11] It was found that the calcification of the arteries could potentially cause misuse of the sphygmomanometer since the calcified arteries would make it more difficult to compress.

Currently, there are no guideline therapies established to treat Mönckeberg's arteriosclerosis. There have been more studies as of recently to learn more about the disease and potential pharmacological managements. Recent studies are showing potential emerging therapies that can help treat arteriosclerosis. A therapy using vasostatin-1, which is a chromogranin A derived peptide, has shown potential in helping treat Mönckeberg's arteriosclerosis.^[12]There are still further discussions and trials needed to help define treatment goals for Mönckeberg's arteriosclerosis.

There are some recommendations for the clinical treatment for people who have complications related to Mönckeberg's arteriosclerosis. Specifically for people with underlying phosphate disorders, the use of phosphate binders, low-dose vitamin D, calcimimetics, magnesium, bisphosphonates, sodium thiosulfate, and aldosterone antagonists have been proposed. Lowering calcium and phosphate levels in people with calciphylaxis, along with increasing hemodialysis and treating potential ischemic necrosis is also recommended.^[13]

Since Mönckeberg's arteriosclerosis is more commonly associated with individuals that have diabetes mellitus and chronic kidney disease, prevention methods can be associated with those disease states. The most fundamental therapeutic goal in prevention would be to lower an individuals risk of cardiovascular events. This can be done by eliminating or controlling risk factors such as smoking or tobacco use, obesity, lack of physical activity, diabetes, hypertension, chronic kidney disease, chronic inflammatory conditions, systemic lupus erythematosus, and hypercholesterolemia.^[14]