Posted by James
Calcium is a key regulator factor in secondary HPT progression. Low serum calcium levels decrease the activation of the Calcium-Sensing Receptor (CaSR), a plasma membrane G-protein coupled molecule that allows parathyroid cells to sense calcium in the extracellular fluid, thus greatly promoting PTH synthesis and secretion. In contrast, hypercalcemia activates the CaSR, rapidly suppressing secondary HPT. Recent evidence suggests that signaling through the CaSR plays an important role on parathyroid hyperplasia. Moreover, calcium-depending signaling through the CaSR may prevent parathyroid hyper- plasia even in tissues that are not-responders to vitamin D. The extracellular calcium concentration may also regulate the level of PTH mRNA and parathyroid cell proliferation. Moreover, calcium regulates VDR mRNA and protein expression in parathyroid cells independently of 1,25(OH)2D. Clearly, serum calcium levels could also indirectly regulate PTH levels through a feedback of 1,25(OH)2D on the parathyroid glands.
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Posted by James
Hyperphosphatemia due to decreased glomerular filtration rate is an important factor in the pathogenesis of secondary HPT. Elevated serum phosphate levels induce secondary HPT through indirect and direct mechanisms. In addition, hyperphosphatemia inhibits 1,25(OH)2D production, with subsequent hypocalcemia.
The direct effects of phosphorus have been demonstrated both in vitro and in vivo studies. High phosphorus concentrations stimulate PTH secretion in intact rat parathyroid glands. Unfortunately, the in vitro effects of phosphorus on PTH secretion could be observed in intact parathyroid tissue preparations, but not isolated, dispersed parathyroid cells. Recently, several studies have shown that phosphate may regulate parathyroid function at post-transcriptional level, as it improves PTH mRNA stability through binding of parathyroid cy- tosolic proteins to the 3′-UTR and especially to the terminal 60 nucleotides of PTH mRNA.
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Posted by James
Vitamin D metabolism
Cholecalciferol (vitamin D3) and ergocalciferol (vitamin D2) derive from dietary sources (animal and fish liver, eggs, fish oils). Cholecalciferol is also produced in the skin from 7-dehydrocho- lesterol (pre-vitamin D3), through the nonenzymatic effect of sunlight ultraviolet B rays (UVB, wavelengths 295-305 nm). 7- dehydrocholesterol is mostly stored in the cytoplasm of cells at the dermal-epidermal border and the effectiveness of its conversion to cholecalciferol is related to the amount of photochro- matic energy entering the skin. Photochromatic energy penetrating the skin greatly depends from the incident angle of UVB rays: in winter, the shallow incident angle of sunlight results in lower energy reaching the epidermis and dermis and, therefore, in lower production of vitamin D3.
Cholecalciferol, ergocalciferol are hydroxilated at carbon 25 in the liver and at carbon 1 in kidney tubules thanks to enzymatic systems including cytocrome P-450 and located at the inner mitochondrial membrane. PTH and hypophosphatemia enhance the activity of renal 1 a-hydroxylase, but not that of liver 25-hydroxylase.
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Posted by James
Spinal Osteoarthritis is characterized by degenerative processes in the spine (spondylosis). A large variety of different shapes can be seen on X-rays. Height reduction of the intervertebral disk space, sclerosis of the endplates, and marginal vertebral osteophytes are typical for osteochondrosis inter- vertebralis whereas normal disk space and submarginal spondylophytes is characterizing spinal osteoarthritis. Because of this additional bone, the shape of the vertebrae changes: wedge shape or concave shape. While degenerative processes are associated with the above described os- teo- and spondylophytes as well as with height reduction of the intervertebral disc space (in case of osteochondrosis), those bone structures are usually not found in cases of osteoporotic vertebral fractures
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Posted by James
Objective quantification of a vertebral fracture can be performed with morphometric measurements. Using a ruler, you can measure the anterior, middle, and posterior heights of the vertebral bodies on a plane X-ray film or digitally on screen (Figure 4). To calculate the grade of fracture, you divide each the anterior and middle height by the posterior height and multiply them with 100. The result is the percentage of deformity. Crushed fracture is defined as a fracture in which the posterior edge of the vertebral body is almost always involved. In order to calculate a crushed vertebra you divide the posterior height with the posterior height of the adjacent vertebral body above and/or below.
A vertebral body is called fractured if the a/p, m/p or p/p height ratio is D80%. This definition was applied in nearly all big international intervention studies and in big epidemiological studies (EVOS, EPOS).
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Posted by James
Osteoporotic vertebral fractures are characterized by end plate deformities of different shape. Increased activity of osteoclasts generates increased numbers of Howship’s resorption lacunae on the surface of bone. Resorption first affects horizontal tra- beculae leading to a deterioration of the trabecular network. This increases the risk of trabeculae buckling, and consequently, vertebral endplates fracture. Deterioration leads to different shapes: wedge, concave, biconcave, or crushed. The diagnosis and classification of the shape of a vertebral fracture should be followed by the quantification of the fracture. Several approaches exist, but only two are important: a semi- quantitative and a morphometric analysis.
Semi-quantitative vertebral fracture analysis
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Posted by James
During the basic diagnostic procedure, it is mandatory to X-ray the patient’s vertebral column in an anterior-posterior and later al projection because for differential diagnostics, it is important to exclude other diseases causing vertebral deformities. In follow-up studies one can reduce X-ray examination to lateral expositions of the spine.
Osteoporotic vertebral fractures occur only in the dorsal and lumbar spine and are extremely rare in the cervical spine and in the upper thoracic vertebral bodies. Therefore X-rays should depict.
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