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Molecular Mechanisms Of Bone Reconstruction In New Dental Implant Technology
Dental Implant Technology
Author: Aurelian Udristioiu
Publisher: Emergency County Hospital TARGU-JIU
10 pages
One time payment: €43.40
Required subscription: Clinical
Type of publication: Dissertation
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Description:

Introduce

 

 

Physiological bone remodeling is a highly coordinated process responsible for bone resorption and formation and is necessary to repair damaged bone and to maintain mineral homeostasis. In addition to the traditional bone cells (osteoclasts, osteoblasts, and osteocytes) that are necessary for bone remodeling, several immune cells have also been implicated in bone disease. Periodontitis is a common disease characterized by resorption of the alveolar bone and is mediated by host responses against multiple commensal bacteria, (1).

 

Previous periodontitis studies have emphasized the importance of host damaging

 

bacteria, including Porphyromonas gingivalis (Pg), which possess high protease and immunosuppressive features (2). Colonization of such tissue-damaging bacteria in the oral cavity is enhanced by streptococci-induced biofilm formation and interactions with multiple commensals.

 

The mechanisms by which commensal species trigger bone resorption associated with periodontitis remain poorly understood. Alveolar bone loss is caused by osteoclast activation through RANKL (receptor activator of NF-κB ligand) signaling. Bacterial components are known to induce alveolar bone resorption by inducing the production of pro-inflammatory cytokines such as tumor necrosis factor-a (TNF-a) and interleukin (IL)-1b, which enhance receptor activator of RANK signaling by up regulation of receptor activator of nuclear factor kappa-B ligand (RANKL) and down-regulation of osteoprotegerin (OPG).

 

Previous studies emphasized the importance of neutrophils in the early phase of periodontitis development.

 

These include studies demonstrating that IL-17 affects alveolar bone resorption by inhibiting the expression of EDIL3, which prevents neutrophil recruitment at the oral bone absorption site in rodent models (3). Osteoprotegerin (OPG)2 is a soluble decoy receptor for RANKL and a physiological negative regulator of osteoclastogenesis; loss of functional OPG in mice results in animals with osteoporosis (brittle bones due to excessive osteoclastogenesis (4).

 

In last years, new technical of dental implants had as objective to solve rebuilding dental bone by a continue process of osteo-genesis.

 

 

Laboratory tehnic of preparation samples of patients

 

 

The preparation samples necessary in dental inplant was made after a special manual of maxilo surgery facial, author, Anitua E, Inplant surgerey and prosthesis. Ed. Eduardo Anitua, Puesta al Dia, Publicaciones, Vitoria, 1998.

 

A total of 10 patients (8 males and 2 females), between 50 and 65 years ( mean age 57.5 years) were appropriately informed that them will collected a small volume of blood, 20 cm ³, drown from peripheral vein, using sodium citrate as anticoagulant, harvesting of peripheral blood, 4.5 mL in 4 coagulation tubes of 5 ml capacity, (38% sodium citrate as an anticoagulant, 0.5 ml).

 

-After a short time, the 4 vacuetes of cagulation with 5 ml blood have been 8 minutes centrifugation at 4500 revs per minute (280 G), in special equipment for this tehnique.

 

-From each 4 tubes of plasma will be extracted from the surface of the tube, 500 microliters plasma with automatic pipette, and will release a container of wastes.

 

-With the same pipette from each tube, from the middle layer, extract plasma, 500 microliters plasma in biochemistry tube labeled with the number 2, (with no anticoagulant or additive, (0.5 ml x 4 = 2 ml, plasma rich in growth factors).

 

-With another pipette of 100 micro-liters capacity, of 3 times from each tube are aspirated the plasma layers remaining in the 4 tubes and it is delivered in biochemistry tube which is labeled with number 1. (4 x 300 microliters = 1.2 ml, layer rich in lymphocytes and megakaryocyte).

 

The plasma delivered in biochemistry dry vacuetts, were kipped for time a 30 minutes, in a thermostat at 37 C*, for to obtain auto-homolougous fibrin for to be used in seal at post-extraction site, to which were added proper dental bone powder filings. The patients, after 24 weeks from extraction with the alveolus sealing, made the CT scan for the evaluation of regenerated new bone density.

 

All patients were registered with very good results in building dental bone and followed a classic technical method of surgery maxilo-facial inplant.

 

 

Role of plasma cells and bone cells in osteogenesis of dental implant

 

 

A biotechnological alternative to accelerate alveolar bone regeneration is filling the post-exstraction alveolus with proper dental bone powder filings and preparation plasma, reach in B and T lymphocytes, monocytes, thrombocytes, megakariocytes and growth factors (PRGF). PRFG consist of small volume of platelet-rich plasma obtained and prepared rapidly and in simple manier from a patents own blood (6). In time the results provided a strong evidence for a sequential physiologic mechanism through which superficial zone(SZ) chondrocytes gain access to active transforming growth factor β (TGF-β, (7). More recently, it was reported that the reversal cells are from the osteoblast lineage, based on cell morphology, positive expression for alkaline phosphatase, and the absence of the monocyte macrophage marker MOMA-2 (monocyte + macrophage antibody-2) on these cells (8).

 

 

T-cells and B-cells

 

 

T- and B-lymphocytes are central components of the adaptive immune system that facilitate recognition and destruction of pathogens. Mice lacking either B- or T-cells have osteoporotic bones, suggesting that these immune cells participate in the maintenance of bone homeostasis during basal physiology. Mechanistically, mature B-cells produce >50% of total bone marrow-derived osteoprotegerin (OPG), which would contribute significantly to restraining osteoclastogenesis during normal physiology. However, the role of T-cells in regulating bone remodeling during homeostasis is less clear, (9).

 

 

Megakaryocytes

 

Derived from hematopoietic stem cells, megakaryocytes reside within bone marrow and produce thrombocytes (known as platelets) that are essential for normal blood clotting. In vitro, megakaryocytes enhance osteoblast proliferation and differentiation, express receptor activator of NF-κB ligand (RANKL) and OPG, and secrete an unknown soluble anti-osteoclastic factor. Overall, these data suggest that megakaryocytes have the potential to direct resorption and formation arms of bone remodeling, (10).

 

 

Osteoclasts

 

 

Osteoclasts are terminally differentiated myeloid cells that are uniquely adapted to remove mineralized bone matrix. These cells have distinct morphological and phenotypic characteristics that are routinely used to identify them, including multi-nuclearity and expression of tartrate-resistant acid phosphatase and the calcitonin receptor. CSF-1 (colony-stimulating factor 1; also known as macrophage colony-stimulating factor) and RANKL are critical cytokines required for survival, expansion, and differentiation of osteoclast precursor cells in vitro (11). Despite the current knowledge of transcription factors involved in osteoclastogenesis, the definitive physiological in vivo osteoclast precursor in mice and humans remains elusive. (12).

 

 

 

Osteoblasts

 

 

Osteoblasts are specialized bone-forming cells that express parathyroid hormone (PTH) receptors and have several important roles in bone remodeling: expression of osteoclastogenic factors, production of bone matrix proteins, and bone mineralization (13). In vitro, phenotypic osteoblast heterogeneity is associated with cell differentiation (14). The stage of osteoblast differentiation also influences the functional contribution of these cells to in vivo bone remodeling.

 

 

 

Also, osteoblasts develop from pluripotent mesenchymal stem cells that have the potential to differentiate into adipocytes, myocytes, chondrocytes, and osteoblasts under the direction of a defined suite of regulatory transcription factors. Osteoblast differentiation is controlled by the master transcription factor RUNX2 (runt-related transcription factor 2; also known as CBFA1 (core-binding factor A1)), RUNX2 null mice have a cartilaginous skeleton and completely lack mineralized tissue due to arrest of osteoblast maturation (15,16).

 

 

Disscution of Process Bone Remodeling:

Bone remodeling occurs over several weeks and is performed by clusters of bone-resorbing osteoclasts and bone-forming osteoblasts arranged within temporary anatomical structures known as "basic multicellular units" (BMUs). Traversing and encasing the BMU is a canopy of cells that creats fates a bone-remodeling compartment (17).

 

Daily activity places ongoing mechanical strain on the skeleton, and it is thought that osteocytes sense changes in these physical forces and translate them into biological signals that initiate bone remodeling. Damage to the bone matrix (or limb immobilization ) results in osteocyte apoptosis and increased osteoclastogenesis (18). Under basal conditions, osteocytes secrete transforming growth factor β (TGF-β), which inhibits osteoclastogenesis.

 

Focal osteocyte apoptosis lowers local TGF-β levels, removing the inhibitory osteoclastogenesis signals and allowing osteoclast formation to proceed (19). Following mineralization of the bone matrix, these entombed cells are called osteocytes and form a network extending throughout mineralized bone.

 

During bone formation, a subpopulation of osteoblasts undergoes terminal differentiation and becomes engulfed by unmineralized osteoid, at which time they are referred to as osteoid-osteocytes (20). Osteocytes are cocooned in fluid-filled cavities (lacunae) within the mineralized bone and are highly abundant, accounting for 90–95% of all bone cells (21). Osteocytes have long dendrite-like processes that extend throughout canaliculi (tunnels) within the mineralized matrix.

 

These dendrite-like processes interact with other osteocytes within mineralized bone and also interact with osteoblasts on the bone surface (22). Osteocytes respond to mechanical load, and this network is thought to be integral in the detection of mechanical strain and associated bone microdamage (microscopic cracks or fractures within the mineralized bone) that accumulates as a result of normal skeletal loading and fatigue (23). Data have been obtained that support the idea that osteocytes initiate and direct the subsequent remodeling process that repairs damaged bone.

 

 

Osteomacs are resident tissue macrophages that reside on or within three cells of endosteal and periosteal surfaces. In human bone, osteomacs can be identified by expression of the myeloid marker CD68, their distinctive stellate morphology, and location in close proximity to bone surfaces (24). In vitro, osteomacs are required for full functional differentiation, including mineralization, of osteoblasts, [Figure 1],(25).

 

 

 

The calciotropic hormone PTH is an endocrine remodeling signal generated to maintain calcium homeostasis. PTH is secreted by the parathyroid glands in response to reduced serum calcium and acts peripherally on kidneys and bone and indirectly on the intestine to maintain serum calcium homeostasis. In the bone microenvironment, PTH activates a seven-transmembrane G-protein-coupled receptor, the PTH receptor, on the surface of osteoblastic cells (26). Binding of PTH to its receptor activates protein kinase A, protein kinase C, and calcium intracellular signaling pathways in these cells (27) and induces a wave of transcriptional responses that produce/modulate secretion of molecules that recruit osteocl.ast precursors, induce osteoclast differentiation and activation, and establish bone resorption.

 

 

Conclusions

 

 

Regenerative therapies such as guided tissue regeneration (GTR) and guided bone regeneration (GBR) are universally accepted as surgical treatments not only for the repair and reconstruction of degraded periodontal tissues but also for quantitative and qualitative enhancement of host bones in localized defects of the alveolar bone.[28]

 

One of the best sources of growth factors in the body is blood platelets. Growth factors such as platelet-derived growth factor (PDGF) and transforming growth factor-β (TGF-β), contained in the α-granules of platelets and released at sites of injury, have been shown to be important in the normal healing of bone, gingiva, and skin.[29]

 

The growing application of dental implants to replace lost teeth coupled with the demand by patients to shorten the healing period following implant installation have also led to vast efforts by researchers to improve the quality of biomaterials and to develop dental implant surfaces with improved macroscopic and microscopic structures that allow enhanced osseointegration, (30).

 

Moreover, some researchers have tried to enhance osteogeneration rate in the peri-implant bones by employing biological factors, especially PDGFs which are typically delivered as PRP or plasma rich in growth factor (PRGF), (31,32).

 

 

Reference

 

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2.Darveau, R.P. Periodontitis: a polymicrobial disruption of host homeostasis. Nat. Rev. Microbiol 2010; 8: 481–490.

 

3.Eskan MA, Jotwani R, Abe T, Chmelar J et al. The leukocyte integrin antagonist Del-1 inhibits IL-17-mediated inflammatory bone loss. Nat. Immunol 2012; (13), 465–473.

 

4.Simonet WS1, Lacey DL, Dunstan CR, Kelley M, Chang MS. Osteoprotegerin: a novel secreted protein involved in the regulation of bone density. Nature 1999; 397; 315–323.

 

5.Michael B. Albro, Robert J. Nims, Alexander D. Cigan, Kevin J. Yeroushalmi. Biophysical Journal 2013; (104)8; 1794-1804.

 

6.Li S, Zhai Q, Zou D, Meng H et all. A pivotal role of bone remodeling in granulocyte colony stimulating factor induced hematopoietic s. J Cell Physiol. 2013;228(5):1002-1009.

 

7.Tang Y1, Wu X, Lei W, Pang L, Wan C. TGF-beta1-induced migration of bone mesenchymal stem cells couples bone resorption with formation. Nat Med. 2009;15(7):757-65.

 

8.Everts V1, Delaissé JM, Korper W, Jansen DC, Tigchelaar-Gutter W. The bone lining cell: its role in cleaning Howship's lacunae and initiating bone formation. J Bone Miner Res. 2002 Jan;17(1):77-90.

 

9. Li Y, Toraldo G, Li A, Yang X,et al. B cells and T cells are critical for the preservation of bone homeostasis and attainment of peak bone mass in vivo. Blood May 2007; (109) 9: 3839-3848.

 

10.Kacena MA, Shivdasani RA, Wilson K, Xi Y, Troiano N.Megakaryocyte-osteoblast interaction revealed in mice deficient in transcription factors GATA-1 and NF-E2. J Bone Miner Res. 2004;19(4):652-60.

 

11.Lacey DL, Timms E, Tan HL, Kelley MJ, Dunstan CR. Osteoclast Differentiation and Activation. Cell 1998; 93; 165–176.

 

12. Arai F , MiyamotoT, Ohneda O, Inada T, Sudo T. J. Exp. Med. 1999;190; 1741–1754.

 

13.Karsenty G. Transcriptional control of skeletogenesisAnnu Rev Genomics Hum Genet. 2008;9:183-96

 

14.Gori F, Hofbauer LC, Dunstan CR, Spelsberg TC. Khosla S. Osteoblasts cell differentiation. Endocrinology 2000; 141; 4768–4776.

 

15.Komori T1, Yagi H, Nomura S, Yamaguchi A, Sasaki K. Targeted disruption of Cbfa1 results in a complete lack of bone formation owing to maturational arrest of osteoblasts. Cell 1997; 89; 755–764.

 

16.Corral DA, Amling M, Priemel M, Loyer E,et al. Dissociation between bone resorption and bone formation in osteopenic transgenic mice. Proc. Natl. Acad. Sci 1998; 95: 13835–13840.

 

17.Hauge EM, Qvesel D, Eriksen EF, Mosekilde L, Melsen F. Cancellous bone remodeling occurs in specialized compartments lined by cells expressing osteoblastic markers. J Bone Miner Res. 2001;16(9):1575-82.

 

18.Aguirre JI, Plotkin LI, Stewart SA, Weinstein RS, Parfitt AM. Osteocyte apoptosis is induced by weightlessness in mice and precedes osteoclast recruitment and bone loss. J Bone Miner Res. 2006;21(4):605-15.

 

19.Heino TJ, Hentunen TA, Väänänen HK. Osteocytes inhibit osteoclastic bone resorption through transforming growth factor-beta: enhancement by estrogen. J Cell Biochem 2002;85(1):185-97.

 

20.Palumbo C. A three-dimensional ultrastructural study of osteoid-osteocytes in the tibia of chick embryos. Cell Tissue Res 1986;246(1):125-3122.

 

21.Bonewald LF. Osteocytes as dynamic multifunctional cells. Ann N Y Acad Sci. 2007;1116:281-290.

 

22.Kamioka H1, Honjo T, Takano-Yamamoto T. A three-dimensional distribution of osteocyte processes revealed by the combination of confocal laser scanning microscopy and differential interference contrast microscopy. Bone 2001;28(2):145-149.

 

23.Verborgt O, Tatton NA, Majeska RJ, Schaffler MB. Spatial distribution of Bax and Bcl-2 in osteocytes after bone fatigue: complementary roles in bone remodeling regulation?.J Bone Miner Res 2002; 17; 907–914.

 

24.Liza J. Raggatt, Nicola C. Partridge. Cellular and Molecular Mechanisms of Bone Remodeling. The Journal of Biological Chemistry 2010;285; 25103-25108.

 

25.Raggatt L J, Partridge N C J., American Society for Biochemistry and Molecular Biology, Biol. Chem 2010;285:25103-25108.

 

26.H Juppner, AB Abou-Samra, M Freeman, XF Kong, E Schipani. A G protein-linked receptor for parathyroid hormone and parathyroid hormone-related peptide. Science 1991: 254(5034): 1024-1026.

 

27.Swarthout JT, D'Alonzo RC, Selvamurugan N, Partridge NC. Parathyroid hormoNe-dependent signaling pathways regulating genes in bone cells. Gene 2002;282(1-2):1-17.

 

28.Hammerle CH, Karring T. Guided bone regeneration at oral implant sites. Periodontol 2000;1998(17):151–75.

 

29.Lynch SE. Bone regeneration techniques in the orofacial region. In: Lieberman JR, Friedlaender GE, editors. Bone regeneration and repair biology and clinical application. Totowa: Humana; 2005. pp. 359–90.

 

30.Misch CE. Rationale for Dental implants. In: Misch CE, editor. Contemporary Implants Dentistry. 3rd ed. St. Louis: Mosby Elsevier 2008; 3: 3–25.

 

31.Mazor Z, Peleg M, Garg AK, Luboshitz J. Platelet-rich plasma for bone graft enhancement in sinus floor augmentation with simultaneous implant placement: Patient series study. Implant Dent. 2004; 13: 65–72

 

32.Kim SG, Kim WK, Park JC, Kim HJ. A comparative study of osseointegration of Avana implants in a demineralized freeze-dried bone alone or with platelet rich plasma. J Oral Maxillofac Surg. 2002;60:1018–25.

 

 

About the publisher:

- My Book written in Clinical Laboratory Medicine, “ Hematological and Metabolical Aspects from Laboratory Medicine” , confirm the aria of my interest in discovery of carcinogenesis mechanisms, especially in onco-haematology field, Leukemia.

Seller www.amazon.com   

Also, my new e-Book: e-BOOK: Hematological and Metabolical Aspects of Laboratory Medicine (Hematological and Metabolical Aspects from Laboratory Medicine) ( Second Edition ) [Large Print] [Paperback].

Publisher: Aurelian Udristioiu, 2 edition (September 9, 2013) Full Color on White paper, 122 pages. ISBN-13: 978-1492186816 (CreateSpace-Assigned) ISBN-10: 1492186813, BISAC: Medical / Laboratory Medicine, USA. Sold by www.amazon.com   

Please, see the Blog of my Medical Book : http://aurelianudristioiu.blogspot.com   

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RECENT WORK OF RESEARCHES

 

1. Udristioiu A. The Assessment of Uncertainty in Measurement of Cholesterol; A Model of Calculation. Biophysical Journal; Volume 96, Issue 3, Supplement 1, February 2009; Page 504a.

2. Udristioiu A, Florescu Cristina, Popescu Manuela Andrei. “High Concentration of anaerobic ATP implicated in aborted apoptosis from CLL”. LabMedicine, American Journal of Clinical Pathology-ASCP, Manuscript 09-08-LM-S-SCI-0122R1, Published in 04-05/2010.

3. Aurelian Udristioiu. First Hematological Signal of Latent Anemia to Aging Population. Nature Publishing Group. Advance Search 0.1038 npre 2009.3285.1. Creative Common Attribution 3.0 License, accepted for the work online posted.

4. Udristioiu A, Cojocaru M, Florescu C. Screening Tests for Latent Anemia in Hospitalized Adults Over 65.   LabMedicine, American Journal of Clinical Pathology-ASCP, Manuscript  09-11-LM-S-SCI-0156.R1,  Published  in 07-05/2010.USA American Journal of Clinical Pathology p-ISSN: 0002-9173 ICV 38.53 LabMedicine ; Ascp Press) , Impact Factor ISI, IF = 2.853 , 18 Index Copernicus Journals Master List 2006.

5. PHENOTYPIC AND GENOTYPIC CHARACTERIZATION OF ANTIBIOTIC RESISTANCE PATTERNS IN ACINETOBACTER BAUMANNII STRAINS ISOLATED IN A ROMANIAN HOSPITAL. MANUELA-ANDA RADU-POPESCU1*, SILVIA DUMITRIU2,SIMONA ENACHE-SOARE3, GABRIELA BANCESCU2, AURELIANUDRISTOIU4, MANOLE COJOCARU5, CODRUTA VAGU6

1 University of Medicine and Pharmacy “Carol Davila, Faculty of Pharmacy, Department of Microbiology, Traian Vuia 6, Sect. 2, 020956,Bucharest, Romania. 6“Stefan S. Nicolau” Virology Institute, Bucharest, Romania. FARMACIA 2010; (57); 3: 420-427 IMPACT FACTOR ISI THOMSON 0.144 .

6. Moleular Biological  Tchiniques  user for identification  of Candida SPP. MANUELA-ANDA RADU-POPESCU1*, SILVIA DUMITRIU2, SIMONA ENACHE-SOARE3,  AURELIAN UDRISTOIU4. 1 University of Medicine and Pharmacy “Carol Davila, Faculty of Pharmacy. FARMACIA 2010; (58); 4: 422-429

7. Udristioiu A. Role of Mg2+ ion as cofactor ATP in assurance of energetic environment cells( Abstract). Magnesium Research 2011; 24 (1): 22-6.

8. -Aurelian Udristioiu, Radu G. Iliescu, Cristina Popescu. Variability of bilirubin values in serum samples with high triglycerides; interference or congenital liver syndromes. J Biosci Tech Volume 2, Issue 4 (JULY 2011).

9. Aurelian Udristioiu¹*,Radu G. Iliescu², Lucian Udristioiu¹ and Manole Cojocaru. A new approach of abnormal apoptosis as a cause of autoimmunity and malignancy. Biotechnology and Molecular Biology Review Vol. 6(8), pp. 166-171, November 2011 . Available online at < http://www.academicjournals.org/BMBR>

10. Aurelian Udristioiu, Cristina Popescu, Manole Cojocaru, Sorina Comisel, Valentina Uscatescu. Relation between LDH and Mg as Factors of Interest in the Monitoring and Prognoses of Cancer. Journal of Bioanalysis & Biomedicine. Ref.:  Ms. No. JBABM-11-48R1 accepted on Jan 27, 2012

11. UDRISTIOIU A. Florescu C, Popescu C, Cojocaru M "Significance of Neutrophil Alkaline Phosphatase versus Isoenzymes ALP in Acute or Chronic Diseases,"accepted for publication in LabMedicine, LabMedicine Manuscript 11-03-LM-U-MR-0052.R2/11/12/2011.

12. Aurelian Udristioiu¹, Radu Iliescu ², Manole Cojocaru³. Errors in Counting Platelets in Hemodialysis Patients by Use of Optical Microscopy. Review of Applied Physics (RAP) Volume 2 Issue 1, March 2013; p: 17-22

13. Aurelian Udristioiu¹, Radu Iliescu ², Manole Cojocaru³. Energetic Levels of Metabolic Pathways in Malignant B and T Cells Mini-Review. Advances in Chemical Science Volume 2 Issue 4, December 2013; 2; 90-95

14. Aurelian Udristioiu¹, Manole Cojocaru² Hemolytic Anemia Drugs Induced by Antihypertensive Agents: A case of Laboratory. 13 Scholars Journal of Medical Case Reports ISSN 2347- 6559. Sch J Med Case Rep 2013; 1(1):8-11

15. Aurelian Udristioiu1*, Radu G. Iliescu2, Manole Cojoraru Molecular mechanisms of bone reconstruction in new dental implant technology. Integrated Journal of British. Volume 1 2014 Issue 1(5-6), pg: 1-7; IJBRITISH.

WRITEN BOOKS:

1.Aurelian Udristioiu. Cicloergometrul si Sanatatea. Ed. Medicala 1990, Bucuresti. ISBN: 973-39-01105-9; Formatul 16/10 x 100; Nr pagini: 78.

2.Aurelian Udristioiu. “Bioenergetica Celulara si Maligna” Ed. Academica Brancusi 2002, Targu Jiu, Bun de tipar, Bucuresti, Tipografia Everest 2001; ISBN 973 85342-6-7; Formatul 16/14 x 100; Nr. Pagini: 307.

3. Aurelian Udristioiu, Manole Cojocaru, Radu Iliescu., Hematological and Metabolic Aspects from Laboratory Medicine" (ISBN 978-3-8473-0775-4). LAP LAMBERT Academic Publishing GmbH & Co. KG Heinrich-Böcking-Str. 6-8 , 66121, Saarbrücken, Germany, 2012.

4. Book title: Renal Diseases / Book 2 (ISBN 979-953-307-704-7). Chapter title: Variability of Biological Parameters in Blood Samples between Two Consecutive Schedules of Hemodyalsis

Authors: Aurelian Udristioiu, Manole Cojocaru, Victor Dumitrascu, Daliborca Cristina Vlad, Alexandra Dana Maria Panait and Radu Iliescu, Publishing Group 2011., Volume 2, Issue 4 (JULY 2011)

5. e-BOOK: Hematological and Metabolical Aspects of Laboratory Medicine (Hematological and Metabolical Aspects from Laboratory Medicine) ( Second Edition ) [Large Print] [Paperback].

 

Publisher: Aurelian Udristioiu, 2 edition (September 9, 2013) Full Color on White paper, 122 pages. ISBN-13: 978-1492186816 (CreateSpace-Assigned) ISBN-10: 1492186813, BISAC: Medical / Laboratory Medicine, USA. Sold by www.amazon.com  

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