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PubMed2006

[The effect of alendronate on arterial calcification in rat model].

OBJECTIVE: To study the effect of alendronate on artery calcification in rats. METHODS: (1) 4-week SD male rats were randomly divided into 3 groups: alendronate group (AL, n = 6), calcification group (CA, n = 6) and normal group (N, n = 6). In AL and CA group, artery calcification of rat was established by subcutaneous injection of vitamin D3 (300,000 U x kg(-1) x d(-1) for 3 days) and Warfarin (15 mg x 100 g(-1) x 12 h(-1) for 4 days); In AL group, at 4 days before establishment of artery calcification, alendronate (1 mg x kg(-1) x 24 h(-1)) was administered with subcutaneous injection and continued to be given to the end of the study. Abdominal aortae were collected for paraffin section and stained with von Kossa staining to observe the area of calcification. (2) Rat aortic vascular smooth muscle cells (VSMC) were cultured in vitro with tissue explant. All cells were divided into 5 groups: normal group, calcification group (control group), and alendronate 10(-9), 10(-7) and 10(-5) mol/L group. Before inducing calcification, alendronate 10(-9), 10(-7) and 10(-5) mol/L group were individually pre-treated with final concentrations of 10(-9), 10(-7) and 10(-5) mol/L alendronate for 24 hours. Beta-glycerophosphate were then added in the calcification group and in all the alendronate groups to induce VSMC calcification. All cells were cultured for 14 days. Cell crawling slice was applied to Alizarin red S staining to observe VSMC calcification. Colorimetric method was applied to measure the contents of Ca2+, cell proteins, and ALP activity. The ratio of contents of Ca2+ and cell proteins was cell calcium deposits. Cell proliferation was measured with tetrazolium salt (MTT) method. RESULTS: (1) With von Kossa staining the black deeply stained structure was found to be decreased in AL group. (2) As compared with the control group, in all the alendronate groups, showed that the number of calcium nodules [(6.8 +/- 2.7, 6.2 +/- 4.2, 5.3 +/- 2.4) % vs (7.4 +/- 3.8)%], and cell calcium depositions [(5.2 +/- 1.2, 4.8 +/- 1.7, 3.5 +/- 1.8)% vs (5.6 +/- 1.6)%], cell ALP activity and cell proliferation decreased significantly and dose-dependently. CONCLUSION: Alendronate can inhibit the artery calcification in rats.

Alendronate↗
PubMed1996

Modifications induced by atherogenic diet in the capacity of the arterial wall in rats to respond to surgical insult.

A study was made of events occurring in the arterial wall of the rat after administration of an atherogenic calcification-inducing diet and of vascular response in a model of combined metabolic aggression (atherogenic, calcification-inducing diet) and surgical aggression (adventitial resection). Female Sprague-Dawley rats were fed an atherogenic, calcification-inducing diet for 24 consecutive days, after which half the rats returned to standard diet (group I, n = 12) and the other half (group II) underwent resection of the adventitia on a segment of common iliac artery on day 25 before returning to standard diet. Normolipemic rats and rats that underwent adventitial resection without the atherogenic, calcification-inducing diet were used as the control groups. The rats were killed at 10 min, 1 and 24 h, 5, 14, 21, 30, 50, 70, 120 and 180 days. Morphologic studies were made with light microscopy and electron microscopy (scanning and transmission), as well as biochemical studies. Monocyte adherence and infiltration of the arterial intima, thickening of the subintimal space, the presence of monocyte-macrophages, calcification in the medial layer, intense adventitial fibrosis, and vacuolization of the endothelial cells of the adventitial microvessels were common findings in the two groups receiving the atherogenic, calcification-inducing diet. However, these groups differed in the intensity of calcification: the deep part of the medial layer did not become calcified when the adventitia was resected. Moreover, adventitial regeneration was delayed in group II with respect to the animals that underwent adventitial resection without atherogenic, calcification-inducing diet. We conclude that this diet induced atherosclerotic lesions in the vessel wall and inhibited adventitial regeneration in the rats that underwent resection.

Animals↗
PubMed1988

Ultrastructural study of hypervitaminosis D induced arterial calcification in Wistar rats.

Hypervitaminosis D produces extensive vascular alterations which are similar to Monckeberg's calcinosis. The present study was undertaken to examine early changes in vascular ultrastructure of rats receiving tap water supplemented with either calcium chloride or a relatively low dosage of irradiated ergocalciferol ad libitum for 21 days. Untreated rats received normal tap water ad libitum. A significant increase in serum calcium levels was obtained in hypervitaminosis D treated rats. Calcium deposits were seen near the internal elastic lamina, within new elastic elements and around degenerating smooth muscle cell fragments in the extracellular organic matrix of hypervitaminosis D treated rats. Calcium deposits were not detected in vascular sections from untreated rats or those receiving calcium chloride. A complex pathogenesis of vascular lesions produced by hypervitaminosis is suggested. One possible pathogenic mechanism for calcification of elastic matrix may be via altered microfibrils. Our data support this hypothesis and indicate that much lower levels of vitamin D administration, compared to other reports, produce considerable vascular calcinosis in this experimental preparation. Several hypotheses regarding possible mechanisms of pathologic calcification are discussed.

Animals↗
PubMed1993

Acute injury of the neck: anatomical and pathological basis of pain.

Headache, upper torso and upper limb pain can all originate in lesions of the cervical spine. The pain distribution is similar whether the cause is traumatic or degenerative. Nociceptive fibres are present in many cervical spine structures including the disc annulus, facet joint capsules, muscles, meninges, arteries, nerve roots and dorsal root ganglia. Such nerves are not present in the disc nucleus, facet articular cartilages and the ligamentum flavum. Central nervous connections between the trigeminal nucleus and upper cervical sensory input provide an explanation for some forms of headache and facial pain. This paper focuses on neck sprain from road traffic accidents as a cause of pain. Similar lesions are seen in the cervical spines of those who die immediately and survivors who die some years after a neck injury, from unrelated causes. Both discs and facet joints are injured. The common disc injury is a "rim lesion" or transverse tear near the anterior vertebral rim. It is caused by distraction and shearing in sudden extension. Both the posterior disc and the facets are compressed, causing disc contusion or herniation, facet haemarthroses, bruising around the C2 nerve, or fractures of articular processes. Suboccipital vascular congestion and annulus calcification are also seen in the "survivors". Chronic pain develops in 20-40% of the "survivors". The reasons include altered spinal mechanics, neural damage and vascular changes. Management must always start with an accurate diagnosis based on a history and physical examination. Simple investigations such as extension X-rays may reveal vacuum clefts in the same anatomical position as rim lesions. Nuclear scans detect increased uptake at damaged end plates or facet fractures.(ABSTRACT TRUNCATED AT 250 WORDS)

Accidents, Traffic↗
PubMed2003

Uremia induces the osteoblast differentiation factor Cbfa1 in human blood vessels.

BACKGROUND: Bone matrix proteins are expressed in calcified arteries from dialysis patients, suggesting that vascular smooth muscle cells (VSMCs) may transform to osteoblast-like cells. One of the key transcriptional regulators of osteoblast differentiation is Cbfa1. Thus, we hypothesized that this may be a key factor in arterial calcification. METHODS: To test this hypothesis, we examined sections of the inferior epigastric artery from uremic patients for the presence of Cbfa1 and type I collagen and osteopontin by in situ hybridization and immunostaining. We also examined the effect of pooled uremic sera from dialysis patients on the expression of Cbfa1 by reverse transcription-polymerase chain reaction (RT-PCR) in bovine VSMCs in vitro. RESULTS: Cbfa1 and osteopontin were expressed in both the media and the intima in vessels that were calcified, but there was only minimal staining in non-calcified vessels. In vitro studies demonstrated that pooled uremic serum, compared to pooled control human serum induced the expression of Cbfa1 by RT-PCR in bovine VSMCs in a time-dependent, nonphosphorus-mediated mechanism. CONCLUSION: These results support that Cbfa1 is a key regulatory factor in the vascular calcification observed in dialysis patients and is up-regulated in response to many uremic toxins.

Animals↗
PubMed2001

Renal cortical calcification in syngeneic intact rats and those receiving an infrarenal thoracic aortic graft: possible etiological roles of endothelin, nitrate and minerals, and different preventive effects of long-term oral treatment with magnesium, citrate and alkali-containing preparations.

Renal cortical nephrocalcinosis (C-NC) is a rare disorder of uncertain etiology. Using highly inbred (syngeneic) male Lewis rats, we describe the spontaneous occurrence of histologically detectable C-NC in sham operated control rats (Sham; n=12), its aggravation following grafting of the ascending thoracic aorta from a donor rat to the infrarenal aorta of a recipient (ATx; n=12), and differences in C-NC inhibition after 12 weeks of oral administration of magnesium (Mg), citrate and alkali. C-NC is characterized by Kossa-positive areas located in cells of the proximal tubule close to blood vessels and also, to a lesser extent, within glomeruli. After ATx there was vascular overproduction of endothelin (ET-1) but decreased production of nitrate; in renal cortical tissue there was an excess of calcium over Mg and phosphorus and oxalate over citrate. In plasma there was an increase in calcium and creatinine within the normal range. Calcification of tubular cells was eliminated by a preparation containing potassium, sodium and bases (from citrate degradation and bicarbonate) in addition to Mg. Less effective than the latter was Mg-potassium citrate and least effective, Mg citrate. The former treatment also normalized calcemia and urinary nitrate, but only incompletely suppressed ET-1 and had no significant effect on glomerular calcification or tissue and urinary oxalate. Urinary ET-1 excess appeared directly related to the cortical tissue calcium/Mg ratio, and urinary excretion of Mg, citrate and total protein appeared to be inversely related to the severity of C-NC. It was concluded that (1) the highly inbred rat is prone to precipitation of calcium phosphate in the renal cortex; (2) this type of C-NC occurs in close proximity to and within renal vascular tissue and is associated with an imbalance of vasoconstrictors and vasodilators of endothelial origin; (3) effective inhibition of C-NC can be achieved by an alkalinizing combination of Mg, potassium, sodium and citrate, underscoring its utility in the prophylaxis of pathological calcium phosphate deposition. The significance of these findings for the etiology and treatment of clinical disorders with renal and vascular calcification is uncertain and requires further investigation.

Alkalies↗
PubMed2000

Medial arterial calcification and diabetes mellitus.

Medial arterial calcification (MAC) is a frequent vascular finding in patients with type II diabetes mellitus. Morphologically distinct from focal calcifications of atherosclerosis its radiographically distinct tramline pattern is frequently encountered in the arteries of the lower extremities. MAC is inconsistently related to age, duration and therapy of diabetes. In contrast, a strong association with diabetic polyneuropathy and familial aggregation have been documented. Although initially considered benign MAC is now recognized as a strong predictor of cardiovascular morbidity and mortality in diabetic patients. Investigations into MAC pathogenes and into its role in vascular pathophysiology are underway.

Arteriosclerosis↗
PubMed1990

Popliteal aneurysm after total knee arthroplasty. Case reports and review of the literature.

Vascular complications after total knee arthroplasty include arterial occlusion, arterial severance, arteriovenous fistula, and arterial aneurysm. Both a false aneurysm and a true aneurysm of the popliteal artery are described. The false popliteal aneurysm resulted from direct surgical trauma and required excision and repair. The true popliteal aneurysm was unsuccessfully treated with excision, transfemoral thrombectomy, and bypass surgery. Many of the vascular complications after total knee arthroplasty may be preventable and the following prudent guidelines are suggested. Careful preoperative evaluation is critical, including past medical history, palpation of pedal pulses, and review of radiographs to identify abnormal calcification in the vessels. Vascular consultation may be necessary. Should a vascular complication occur, immediate intervention with the advice and assistance of a vascular surgeon is imperative.

Aged↗
PubMed1982

Medial arterial calcification and diabetic neuropathy.

X-ray examinations of the feet, knees, and hands were performed on 20 diabetics with severe neuropathy and 20 diabetics with no evidence of neuropathy but with a similar mean age and duration of diabetes. All were under 53 years old with no clinical evidence of peripheral vascular disease. Medial arterial calcification was much more common and extensive in the patients with neuropathy, occurring in the feet in 15 and in the hands in eight compared with in four (p less than 0.001) and none (p less than 0.001) of the controls respectively. Although there was some correlation between calcification and both proteinuria (p less than 0.05) and proliferative retinopathy (p less than 0.02), the association between calcification and neuropathy (p less than 0.001) was much stronger. Neuropathy, with sympathetic denervation of the smooth muscle of the tunica media, may be important in the aetiology of medial arterial calcification.

Adult↗
PubMed2005

Angiotensin II and aldosterone regulate gene transcription via functional mineralocortocoid receptors in human coronary artery smooth muscle cells.

Inhibition or blockade of the angiotensin-aldosterone system consistently decreases ischemic cardiovascular events in clinical trials. The steroid hormone aldosterone acts by binding to the mineralocorticoid receptor (MR), a ligand activated transcription factor that is a member of the nuclear hormone receptor superfamily. MR binds and is activated by aldosterone and cortisol with equal affinity, but MR activation by cortisol is diminished in tissues that express the cortisol-inactivating enzyme 11-beta-hydroxysteroid-dehydrogenase-2 (11betaHSD2). Although previous studies support that the vasculature is a target tissue of aldosterone, MR-mediated gene expression in vascular cells has not been demonstrated or systematically explored. We investigated whether functional MR and 11betaHSD2 are expressed in human blood vessels. Human coronary and aortic vascular smooth muscle cells (VSMCs) express mRNA and protein for both MR and 11betaHSD2. The endogenous VSMC MR mediates aldosterone-dependent gene expression, which is blocked by the competitive MR antagonist spironolactone. Inhibition of 11betaHSD2 in coronary artery VSMCs enhances gene transactivation by cortisol, supporting that the VSMC 11betaHSD2 is functional. Angiotensin II also activates MR-mediated gene transcription in coronary artery VSMCs. Angiotensin II activation of MR-mediated gene expression is inhibited by both the AT1 receptor blocker losartan and by spironolactone, but not by aldosterone synthase inhibition. Microarray and quantitative RT-PCR experiments show that aldosterone activates expression of endogenous human coronary VSMC genes, including several involved in vascular fibrosis, inflammation, and calcification. These data support a new MR-dependent mechanism by which aldosterone and angiotensin II influence ischemic cardiovascular events, and suggest that ACE inhibitors and MR antagonists may decrease clinical ischemic events by inhibiting MR-dependent gene expression in vascular cells.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed1979

Ectopic calcification in lambs from feeding the plant Cestrum diurnum.

Hypercalcemia and ectopic calcification were induced in 5 lambs by supplementing the diet with the dried leaves of the plant Cestrum diurnum, for 8 to 9 weeks. Lambs developed mineralization of blood vessels, heart, kidneys, and lungs. These tissues were examined by light and electron microscopy. In the vascular tissue there was calcification of elastic fibers in the hyperplastic intima and the media, along with mineralization of mitochondria of aortic smooth muscle cells. Myocardial cells and their mitochondria were mineralized. In the kidney, there was calcification of the epithelium of the distal convoluted tubules and collecting tubules, Bowman's capsule, and the mesangial cells of the glomeruli. In the lung, there was mineralization of the alveolar septal walls and the bronchi and bronchioles. Feeding of the calcinogenic plant to lambs caused extensive soft tissue calcification. Results of the study indicated that degeneration was the early soft tissue lesion in this plant toxicity.

Animals↗
PubMedDate not supplied

Dysembryoplastic neuroepithelial tumor: a clinicopathologic and immunohistochemical study of 11 tumors including MIB1 immunoreactivity.

The dysembryoplastic neuroepithelial tumor (DNT) is a rare, recently recognized neoplasm, characterized by a mixed glial-neuronal cell proliferation. We studied 11 cases of DNT including 6 males and 5 females (age range 2.1-39.4 years, mean 13.8 years). All patients presented with chronic epilepsy of 4.8 years mean duration. Nine tumors were located in the temporal lobe and 2 in the frontal lobe. Four tumors were located on the right side and 7 on the left. All tumors were characterized by a predominant oligodendrocyte-like cell component with intermixed normal appearing neurons and astrocytes. All were focally microcystic and 7 of 9 evaluable tumors were multinodular. Other observed histologic features included a focal arcuate vascular pattern in 7 tumors, calcification in 4 tumors, and a rare mitotic figure in 2 tumors. Necrosis and vascular hyperplasia were not observed in any of the tumors. Cortical architectural disorganization (cortical dysplasia) was observed in 9 of 10 evaluable cases. MIB1 (a marker of cellular proliferation) immunostaining was performed in all 11 tumors and MIB1 indices (number of positive tumor cells/100 tumor cells counted) ranged from 0-0.6 (mean 0.2). Four patients required at least 1 additional surgical procedure for tumor recurrence, related to an incomplete initial excision 2.1-4.4 years after their initial operation. All patients are seizure-free at their last follow-up. DNTs are low grade neoplasms which typically present with chronic epilepsy, are most frequently located in the temporal lobe, and occur most frequently in pediatric patients. Their appearance and association with cortical dysplasia suggest a maldevelopmental origin. The generally slow growth and relatively benign nature of DNT is reflected by their low MIB1 index.

Adolescent↗
PubMed2005

Associations of serum fetuin-A with malnutrition, inflammation, atherosclerosis and valvular calcification syndrome and outcome in peritoneal dialysis patients.

BACKGROUND: Fetuin-A (alpha2-Heremans Schmid glycoprotein) has recently been identified as a circulating inhibitor of calcification and is regulated as a negative acute phase protein. However, its relationships with cardiac valvular calcification and atherosclerosis and outcome have not been evaluated in peritoneal dialysis (PD) patients. METHOD: We performed a prospective follow-up study in 238 PD patients with echocardiography done at baseline to detect cardiac valvular calcification and biochemical analysis performed for serum fetuin-A, albumin and C-reactive protein (CRP). RESULTS: Baseline serum fetuin-A concentration was (mean+/-SD) 0.309+/-0.068 g/l (normal range 0.4-0.95). Across the three tertiles of increasing serum fetuin-A, a significant trend effect was observed for age (P = 0.023), diabetes (P = 0.008), background atherosclerotic vascular disease (P = 0.010), cardiac valvular calcification (P = 0.002), serum albumin (P<0.001), subjective global assessment (P = 0.005) and CRP (P<0.001). Adjusting for CRP and calcium x phosphorus product, every 0.01 g/l increase in serum fetuin-A remained independently associated with a 6% decrease in the risk of valvular calcification (95% confidence intervals, 0.90-0.99; P = 0.028). Furthermore, serum fetuin-A showed a significant decrease across the four groups of patients with increasing components of the malnutrition, inflammation, atherosclerosis/calcification (MIAC) syndrome (P<0.001) and was the lowest among patients with all components of the MIAC syndrome (0.263+/-0.055 g/l) and highest among those who do not have the MIAC syndrome at all (0.338+/-0.063 g/l). Lower serum fetuin-A was associated with greater all-cause mortality (P = 0.0011) and fatal and non-fatal cardiovascular events (P = 0.0017), but its significance was lost when atherosclerotic vascular disease, valvular calcification, inflammation and malnutrition were included in the model. CONCLUSIONS: Serum fetuin-A showed important associations with valvular calcification, atherosclerosis, malnutrition and inflammation, and was linked to mortality and cardiovascular events in PD patients via its close relationships with the MIAC syndrome.

Arteriosclerosis↗
PubMed2000

Association of osteopontin with calcification in human mitral valves.

BACKGROUND: Little is known about the long-standing inflammation leading to calcification within heart valves. Osteopontin, a phosphorylated glycoprotein, is present within atheromatous calcific plagues in response to vascular endothelial injury. The purpose of the study was to investigate whether osteopontin exists in calcific mitral valve leaflets in human beings, and to determine a link between chronic inflammation leading to mitral stenosis and the osteopontin status of mitral valvular tissue. MATERIALS AND METHODS: We reviewed the case histories of 17 patients who underwent mitral valve replacement therapy for mitral stenosis between 1995 and 1997 (8 men and 9 women, mean age 61 years). Hybrid mouse monoclonal immunoglobulin G1 antibodies were used for immunohistochemical detection of osteopontin in the acetone-fixed specimen. The control group consisted of normal mitral valve tissue from cardiomyopathy patients who underwent cardiac transplantation. RESULTS: A weak osteopontin immunoreactivity was present in apparently normal mitral valve tissue obtained from cardiomyopathy patients. All mitral stenosis patients had immunoreactivity (17/17) for osteopontin within calcific deposits of mitral valve tissue. The intensity of osteopontin activity had a strong association with increasing macrophage and calcium aggregations in the mitral valvular tissue. We found no correlation between osteopontin status and clinical features on the prognosis of calcific mitral stenosis. CONCLUSIONS: We conclude that osteopontin coexists with intimal macrophages in calcific human mitral valve tissue. Demonstration of such association between the presence of osteopontin and calcification in human mitral valves is consistent with the hypothesis that calcification in this tissue is, at least in part, an actively mediated phenomenon.

Aged↗
PubMed2000

Foreign-body reaction to dermal sheep collagen in interferon-gamma-receptor knock-out mice.

This study was performed to gain more insight into the role of interferon-gamma (IFN-gamma), a potent macrophage activator, in the foreign-body reaction to hexamethylenediisocyanate-crosslinked dermal sheep collagen (HDSC). Because the results of earlier studies aimed at modulating the foreign-body reaction in AO rats by local or systemic treatment with anti-IFN-gamma were not completely unambiguous, we extended our investigations to IFN-gamma-receptor knock-out (KO) mice. Several parameters (i.e., macrophages, giant cells, T-cells, B-cells, granulocytes, expression of MHC class II, stroma formation, and degradation and calcification of the biomaterial) were compared between wild-type (WT) and KO mice. Remarkably, the foreign-body reaction was very similar in WT and KO mice. In both, giant cells were formed, but in contrast to previous results in AO rats, phagocytosis of HDSC bundles occurred hardly at all up to 9 weeks, and MHC class II expression was minimal. Stroma formation and vascularization were high and calcification occurred. T-cells comprised less than 1%; a few plasma cells were present in the KO mice at later time points. Granulocytes, mainly eosinophils, were present at all explantation time points. Because of the similar results in WT and KO mice, we question whether IFN-gamma plays a role at all in the foreign-body reaction in mice.

Animals↗
PubMed1993

Immunohistochemical demonstration of nerve fibers in pelvic adhesions.

OBJECTIVE: To demonstrate the presence of nerve fibers in pelvic adhesions potentially capable of conducting pain stimuli. METHODS: Pelvic adhesions from 17 patients, ten of whom had a history of pelvic pain, were examined histologically. Routine hematoxylin and eosin stains and immunoperoxidase stains for S100 protein, B lymphocytes, and T lymphocytes were performed. Mesothelial proliferation, presence of calcification and/or psammoma bodies, edema, vascularization, inflammation, fibroblastic proliferation, and collagenization were graded from 0 (absent) to 3 (extensive); their prevalences were compared between patients with and without pelvic pain. RESULTS: Nerve fibers were present in specimens from ten of the 17 patients (five of ten patients with and five of seven without pain). There was no statistically significant difference in the numbers with nerve fibers or in the presence of mesothelial proliferation, calcification and/or psammoma bodies, edema, vascularization, inflammation, fibroblastic proliferation, or collagenization between the groups. In all cases, the infiltrating lymphocytes were T lymphocytes. CONCLUSION: We were able to demonstrate the presence of nerve fibers in pelvic adhesions; however, their presence was not more prevalent among patients with pelvic pain. These findings support the concept that the formation of adhesions has different stages, with the final formation of mature connective tissue with its own vascularization and innervation.

Cell Division↗
PubMed1997

Lipid oxidation products have opposite effects on calcifying vascular cell and bone cell differentiation. A possible explanation for the paradox of arterial calcification in osteoporotic patients.

Atherosclerotic calcification and osteoporosis often coexist in patients, yielding formation of bone mineral in vascular walls and its simultaneous loss from bone. To assess the potential role of lipoproteins in both processes, we examined the effects of minimally oxidized low-density lipoprotein (MM-LDL) and several other lipid oxidation products on calcifying vascular cells (CVCs) and bone-derived preosteoblasts MC3T3-E1. In CVCs, MM-LDL but not native LDL inhibited proliferation, caused a dose-dependent increase in alkaline phosphatase activity, which is a marker of osteoblastic differentiation, and induced the formation of extensive areas of calcification. Similar to MM-LDL, oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (ox-PAPC) and the isoprostane 8-iso prostaglandin E2 but not PAPC or isoprostane 8-iso prostaglandin F2 alpha induced alkaline phosphatase activity and differentiation of CVCs. In contrast, MM-LDL and the above oxidized lipids inhibited differentiation of the MC3T3-E1 bone cells, as evidenced by their stimulatory effect on proliferation and their inhibitory effect on the induction of alkaline phosphatase and calcium uptake. These results suggest that specific oxidized lipids may be the common factors underlying the pathogenesis of both atherosclerotic calcification and osteoporosis.

Alkaline Phosphatase↗