Journal of Dental Implants
   About JDI | Editorial | Search | Ahead of print | Current Issue | Archives | Instructions | Subscribe | Login 
Users Online: 445  Wide layoutNarrow layoutFull screen layout Home Print this page  Email this page Small font size Default font size Increase font size


 
 
Table of Contents
ORIGINAL ARTICLE
Year : 2012  |  Volume : 2  |  Issue : 1  |  Page : 9-14

Nitric oxide level around dental implant: Indicator of an inflammatory process


1 Department of Periodontics, Faculty of Dental Sciences, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India
2 Department of Anatomy, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India

Date of Web Publication24-May-2012

Correspondence Address:
Royana Singh
Department of Anatomy, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-6781.96557

Rights and Permissions
   Abstract 

Aim: The purpose of the present study is to determine the measure of inflammation of nitric oxide (NO) in healthy dental implants and diseased implants.
Materials and Methods: A total 102 subjects constituting of two groups: Tooth and dental implant sites were selected, constituting of healthy and inflamed subgroup. NO levels were spectrophotometrically determined. For comparison Chi square and paired t-test analysis was done. The correlation between NO levels and clinical inflammatory status were analyzed with Spearman's correlation coefficient.
Results: Gradual increase in the GCF and PISF volume was exhibited in the inflamed tooth as well implants. The total NO level was significant higher in the inflamed sites (P<0.05) than the non-inflamed sites in both tooth and the implant sites.
Conclusion: The PISF (peri-implant sulcus fluid) may have a diagnostic potential for reflecting the biological changes around load-bearing endosseous dental implants.

Keywords: Dental implants, inflammation, natural teeth, nitric oxide


How to cite this article:
Durrani F, Ojha U, Singh V P, Singh R. Nitric oxide level around dental implant: Indicator of an inflammatory process. J Dent Implant 2012;2:9-14

How to cite this URL:
Durrani F, Ojha U, Singh V P, Singh R. Nitric oxide level around dental implant: Indicator of an inflammatory process. J Dent Implant [serial online] 2012 [cited 2021 Oct 21];2:9-14. Available from: https://www.jdionline.org/text.asp?2012/2/1/9/96557


   Introduction Top


Dental implants have been remarkably improved in the past half century. When good-quality dental implants and techniques are used, implants show similar cumulative success rates at 10 years after implantation. The 10-year cumulative success rates are about 88% for maxillary and 93% for mandibular implants [1] but some implants are lost as a result of primary failure or by loosening, a mode of failure resulting from implant movement or migration in the bone. [2] Unfortunately, these patients, who are mostly about 60 years old, are still quite young in terms of current human longevity. [3] As a result of failure or loosening of the implants and the longevity of the patients, some patients would later need to be re-implanted. But often the possibilities for revision operations are limited, due to general and local circumstances. [4] The high and increasing number of dental implantations performed [5] is evidence that loosening of dental implants is a common complication affecting thousands of patients annually worldwide.

More recently, criteria for implants were approved by The American Academy of Periodontology in 2000. [6] These include: "1) absence of persistent signs/symptoms such as pain, infection, neuropathies, paresthesias, and violation of vital structures; 2) implant immobility; 3) no continuous peri-implant radiolucency; 4) negligible progressive bone loss (less than 0.2 mm annually) after physiologic remodeling during the first year of function; 5) patient/dentist satisfaction with the implant-supported restoration". [6] Thus the control of etiologic agents that cause onset of peri-implant tissue inflammation plays a critical role in long-term success of endosseous dental implants. Periodontally compromised patients (PCP) present a potentially higher risk for implant failure. The reason for this is that period following such initial peri-implant inflammation, which generally resembles the reversible plaque-related tissue reactions around natural tooth, can induce irreversible destruction of peri-implant tissues. Dental implant studies have demonstrated that any loss of integrity of biological seal of peri-implant tissues is an important factor that may trigger peri-implant soft tissue inflammation and alveolar bone loss (peri-implantitis), which may result in implant failure.

Early recognition of any peri-implant pathology including peri-implant soft tissue inflammation is vital for long-term proper functioning of dental implants.The development of simple and reliable diagnostic tools for early detection of initial peri-implant inflammatory process and prevention of any irreversible host reactions, such as destructive peri-implant disease, may be of particular importance. There is a large body of evidence that NO is involved in several inflammatory disorders. Indeed, virtually every cell and many immunological parameters are modulated by NO. It has been shown that NO can be both pro-inflammatory (immune-stimulatory, anti-apoptotic) or anti-inflammatory (immunosuppressive, pro-apoptotic), host-protective or host damaging during infections. For these reasons NO has been described as "double-edge sword mediator" and this phenomenon is often referred to as the NO paradox.

Menaka, et al., [7] revealed an increase in NO expression in periodontitis and demonstrated that enhanced formation of NO played a significant role in the pathogenesis of periodontitis. Also that the deactivation of NO by activated PMNs as one of the pathomechanisms of disorders in periodontitis. [8]

Thus, the present status of the role of NO in periodontal disease is not clearly defined and this study was therefore undertaken to reveal the involvement of NO in periodontal disease and to see the probability of use of NO estimation as reliable diagnostic tool for early detection of initial peri-implant inflammatory process and, henceforth, chances of implant failure.


   Materials and Methods Top


Patients and samples

Patient participation in this study did not endanger their health. They underwent procedures deemed necessary for their oral health. Participation did not involve them in any extra dental procedures. Participation was voluntary. All patients gave their informed consent. The project was approved by the local ethics committee of the participating institutes.

Gingival crevicular fluid (GCF) sample is an accepted method for evaluation of clinical periodontal status of the natural dentition and for better understanding of pathogenesis of periodontal disease.

Inclusion criteria and selection of participants

The patients were required to be healthy with no allergies or metabolic bone diseases;

No history of antibiotic prior 3 months.

Patients with dental implants and natural teeth preferred in order to minimize the inter-patient variation. However, patients with only implants or teeth were not excluded;

All the patient who were included in the study in clinical periodontal health should have one site of each of the following:

  • Healthy site
  • Gingivitis
  • Periodontitis
  • Dental implant restoration need to be in function for at least six months and
  • Patients attending faculty for periodontal care and implant maintenance


Determination of the clinical status of the soft Tissue

Clinical status of peri-implant soft tissues and clinical periodontal status of natural tooth sites were evaluated by assessing the probing depth (PD), Plaque Index (PI) score, Gingival Index (GI) score, and the Gingival Bleeding Time Index (GBTI). These measurements were used to assess the presence/extent of both periodontal and peri-implant inflammatory destruction. All measurements were performed at four sites around each implant and natural tooth (mesial, distal, buccal, and lingual) and were carried out to the nearest mm using a Michigan 'O' probe. To avoid any volumetric disturbance, all of the clinical measurements were recorded after PISF and GCF sampling.

PISF/GCF sampling

PISF/GCF sampling was performed at the dental implant and natural tooth sites as guided by Rüdin et al., Chapple IL, Atici K et al., and Tözüm TF et al. PISF/GCF samples were obtained according to the method described by Rüdin et al. using standardized paper strips (Periopaper, no. 593525; Ora Flow, Amityville, NY). Briefly following the isolation of the sampling area with sterile cotton rolls, supragingival plaque was removed, and the site was gently air-dried to reduce any contamination with plaque and saliva. Care was taken to minimize the level of mechanical irritation. Paper strips were placed at the entrance of the peri-implant sulcus or natural tooth crevice and were inserted to a standardized depth of 1 mm at each site for 30 s. Samples with evidence of gingival bleeding were not included. To eliminate the risk of evaporation, paper strips were immediately transported for electronic volume determination. PISF/GCF was measured electronically. The PISF/GCF samples were then placed in sterile, wrapped Eppendorf tubes and stored at -20°C until the day of laboratory analysis.

Determination of nitrite Level of PISF/GCF

To each PISF/GCF sample in the Eppendorf tube, 300 μL extraction buffer (10 mmol/L phosphate buffer containing 0.5%,hexadecyltrimethylammonium bromide [HETAB], ph 6.0), was added, and the samples were vigorously mixed for the extraction of nitrite into the buffer. For the determination of nitrite levels, 150 μL of the extract was mixed with 150 μL of freshly prepared Greiss reagent (1% sulfanilamide, 0.1% naphthylethylenediamine dihydrochloride and 2.5% hydrochloric acid) using a microplate. After 10 min of incubation at room temperature, the absorbance of each sample in microplate wells was determined at 540 nm. [9],[10] A standard curve was prepared using sodium nitrite to calculate nitrite concentration in PISF/GCF.

Formula for measurement of nitrite level

Nitrite concentration in samples was calculated by relating the net optical density of the sample to nitrite concentration in standard curve in the following way:


   Results Top


A total of 107 sites in 21 subjects were included in the present cross-sectional study. Of these, 21 patients (with a mean age of 44 years), 10 men and 11 women, had been treated with screw-type endosseous dental implants. Ten of 21 patients had both dental implants and natural teeth; 51 peri-implant and periodontal sites in these patients were measured. Eleven subjects had only either dental implants or natural teeth; 58 sites in these patients were measured. Of the sites, 42 were dental implant sites, while 67 were natural tooth sites with clinical health or some state of inflammation. The descriptive statistical analysis and actual P values are provided in [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6] and [Table 7]. The impact of severity of inflammation on clinical measures, together with descriptive statistical analysis and actual P values, is shown in [Table 8] and [Table 9].
Table 1: Analysis of plaque index of natural teeth and dental implants grouped by state of inflammation

Click here to view
Table 2: Analysis of probing depth of natural teeth and dental implants grouped by state of inflammation

Click here to view
Table 3: Analysis of gingival bleeding time index of natural teeth and dental implants grouped by state of inflammation

Click here to view
Table 4: Analysis of gingival crevicular fluid/peri-implant sulcus fluid index of natural teeth and dental implants respectively, grouped by state of inflammation

Click here to view
Table 5: Analysis of nitrite level of GCF/PISF of natural teeth and dental implants grouped by state of inflammation

Click here to view
Table 6: Analysis of total nitrite concentration of natural teeth and dental implants grouped by state of inflammation

Click here to view
Table 7: Analysis of plaque index and probing index of natural teeth and dental implants grouped by state of inflammation

Click here to view
Table 8: Analysis of plaque index of natural teeth and dental implants grouped by state of inflammation

Click here to view
Table 9: Analysis of nitrite level and total nitrite concentration of natural teeth and dental implants grouped by state of inflammation

Click here to view


For both of the laboratory measures, total and concentration modes of data presentation did not match and presented different trends. While in GCF the total nitrite levels stayed quite stable in all clinical circumstances (periodontal health: 0.050 nmol; gingivitis: 0.053 nmol; periodontitis: 0.052 nmol; P&gt;0.05), GCF nitrite concentration clearly presented a different pattern (periodontal health: 0.433 nmol/μL; gingivitis: 0.159 nmol/μL; periodontitis: 0.051 nmol/μL; P=0.0001). Where dental implant sites were concerned, the PISF total nitrite (P=0.001) was significantly higher. While no difference was observed in any of the laboratory parameters between inflamed GCF and PISF samples, total nitrite level demonstrated a pattern of increase in GCF from healthy natural tooth sites compared to PISF from non-inflamed implant sites. Despite a trend of increase in clinical parameters and the severity of inflammation at moderately/severely inflamed sites, GCF total nitrite levels stayed stable and were not influenced by the severity of clinical inflammation. At dental implant sites, higher PI and GBTI scores were observed at moderately/severely inflamed sites than both the clinically non-inflamed sites (P = 0.0001). Total nitrite levels presented a trend of increase in the inflamed sites compared with the clinically non-inflamed dental implant sites, while slightly inflamed sites demonstrated a significantly increased total nitrite level compared to non-inflamed peri-implant sites (P = 0.004). However, no significant difference was observed between slightly inflamed and moderately/severely inflamed sites (P>0.05). However, no correlation was found for total nitrite level and nitrite concentration at natural tooth and dental implant sites.


   Discussion Top


In addition to the examination of clinical parameters, quantitative and qualitative analysis of GCF samples is an accepted method for the evaluation of early and destructive stages of inflammatory periodontal diseases around natural teeth, while PISF analysis may serve for further clarification of the biologic mechanisms around dental implants and the pathophysiology of peri-implant diseases [11],[12],[13],[14],[15],[16],[17],[18] There is the possibility that these biological fluids may share much in terms of their diagnostic potential and their involvement in the pathogenesis of periodontal or peri-implant disorders. [11],[12],[13],[14],[15],[16],[17],[18] The volumetric findings of the present study support the idea of such a similarity; both the GCF and PISF volumes exhibited clear increases at diseased sites compared to clinically healthy sites, in addition to the similarities between the sites with respect to clinical peri-implant or periodontal parameters. Further, despite the higher PISF volume at non-inflamed sites, no significant difference between PISF and GCF volume could be observed at inflamed sites. Thus, it seems that that PISF and GCF share similar volumetric features in their local response to existing clinical inflammation. It is clear that molecular changes around natural teeth and/or load-bearing dental implants are complex, and a close relationship has been demonstrated between inflammatory status and the molecular pathophysiology. [11],[12],[15],[16] This, in fact, seems to be the main reason for the great interest in GCF and PISF and their potential changes with inflammation. [11],[12],[15],[16],[17],[18],[19] The lack of significant correlations between certain laboratory measures and clinical parameters has been attributed to the lack of a correlation between time of GCF profiling and clinical status. [20],[21],[22] The relatively "early" nature of such laboratory measures (e.g., enzymatic changes in GCF profile), which precede clinically detectable changes, has also been suggested. [22],[23] Thus, analysis of various laboratory-based parameters (e.g., biochemical measures), rather than clinical parameters, may serve for the development of reliable diagnostic tests for early detection of periodontal inflammation. [20],[21],[22] In addition to these, the significant limitations of most clinical parameters (e.g., having subjective elements in reflecting only past events, providing limited information on actual disease status, the potential for missing early signs of disease, lack of 100% specificity and sensitivity, having limited prognostic value) continue to give rise to laboratory-based studies that aim to overcome these limitations. [20],[23]

NO has been considered an important molecular signal in a wide variety of tissues and may play a significant role as a cytotoxic mediator of the nonspecific immune response, with beneficial and harmful effects. [24],[25],[26] Inducible NO synthase (inos) is expressed in response to inflammatory stimuli, resulting in higher amounts of NO production, and much of the share and the diagnostic potential of PISF, the results should be interpreted with caution due to the limited number of samples analyzed. Further studies to evaluate and compare the components of PISF and GCF, especially with respect to the inflammatory process and bone metabolism, are needed to increase our understanding of the role of each component and the diagnostic potential of PISF for peri-implant pathologies as a biological fluid.

Nitrite of body fluids is formed from oxidation of NO produced by inos [25],[26] Increased numbers of inos positive cells have been demonstrated in periodontally diseased tissues. [27],[28],[29],[30] Because of the reactivity of NO and its short life, direct measurement of NO from body fluids has been thought hard to perform. [31] Thus, nitrite, a stable end-product of NO oxidation, has been measured instead. [16],[31] In the present study, using Greiss reactions, increased NO metabolism with peri-implant inflammation, represented by higher PISF nitrite levels at inflamed dental implant sites, compared to healthy ones was observed in patients with edentulous mandibles rehabilitated with overdentures with ball attachments supported by implants. [16] The finding of an increase in PISF NO metabolism at inflamed sites is in line with the previously reported results of a comparative analysis of PISF nitrite levels at inflamed and non-inflamed peri-implant sites in subjects with implant-supported fixed prostheses [16] Based on the previously demonstrated discrepancy between "concentration" and "total activity" modes of data presentation for GCF [17],[33] in the present study, it was not surprising to observe that these two modes of data presentation for GCF were not completely correlated. The same discrepancy was also observed for PISF samples. As concentration expression is affected by the available PISF or GCF volume in a given site, it may be suggested that GCF and PISF share similar volumetric features with respect to the appropriate mode of data presentation, [16],[17],[32] NO metabolism may be affected by force and loading. [16],[33] Thus, besides the inflammatory process, PISF nitrite levels may also be affected by the loading of dental implants. It is possible that the design of the implant-supported prosthesis (e.g., a complete mandibular prosthesis supported by a ball attachment) may affect NO production at dental implant sites and the subsequent PISF nitrite levels. In the present study, two biological fluids, PISF and GCF, were comparatively analyzed. Although the results may shed light on the features of the two fluids, share and the diagnostic potential of PISF, the results should be interpreted with caution due to the limited number of samples analyzed. Further studies to evaluate and compare the components of PISF and GCF, especially with respect to the inflammatory process and bone metabolism, are needed to increase our understanding of the role of each component and the diagnostic potential of PISF for peri-implant pathologies as a biological fluid.


   Conclusions Top


The findings of the present study support the contribution of NO metabolism to the inflammatory process around both natural teeth and dental implants. PISF appears to have diagnostic potential for the discrimination between peri-implant health/disease and for a better understanding of the peri-implant biological mechanisms on a molecular level.

 
   References Top

1.O'Roark WL. Survival rate of dental implants: an individual practitioner's anecdotal review of 25 years of experience. J Oral Implantol 1997;23:90-103.  Back to cited text no. 1
    
2.Curtis DA, Kao R, Plesh O, Finzen F, Franz L. Crevicular fluid analysis around two failing dental implants: A clinical report. J Prosthodont 1997;6:210-4.  Back to cited text no. 2
    
3.Pihakari A, Nevalainen J, Hirvonen A, Mäkelä A. The 2000 dental implant yearbook. Publications of the National Agency for Medicines 1/2001.  Back to cited text no. 3
    
4.Oikarinen K, Raustia AM, Hartikanien M. General and lokal contraindications for endosseal implants-an epidemiological panaromic radiograph study in 65-years old subjects. Community Dent oral Epidemiol 1995;23:114-8.  Back to cited text no. 4
    
5.Kronstrom M, Palmqvist S, Soderfeldt B, Vigild M. Utilization of dental health services among middle-aged people in Sweden and Denmark. Acta Odontol Scand 2002;60:276-80.  Back to cited text no. 5
    
6.Iacono VJ. Dental implants in periodontal therapy. J Periodontol 2000;71:1934-42.  Back to cited text no. 6
    
7.Menaka KB, Ramesh A, Thomas B, Kumari NS. Estimation of Nitric oxide as inflammatory marker in Periodontitis. J Indian Soc Periodontol 2009;13:75-8.  Back to cited text no. 7
[PUBMED]  Medknow Journal  
8.Akopov SE, Kankanian AP. Nitric oxide (NO) inactivation by polymorphonuclear leukocytes as a mechanism for the development of periodontal lesions. Stomatologiia (Mosk) 1996;75:12-4.  Back to cited text no. 8
    
9.Grisham MB, Johnson GG, Gautreaux MD, Beng RD. Measurement of nitrate and nitrite in extracellular fluids: A window to Systemic nitric oxide metabolism. Methods: A Companion to Methods in Enzymology 1995;7:84-90.  Back to cited text no. 9
    
10.Deinzer R, Mossanen BS, Herforth A. Methodological considerations In the assessment of gingival crevicular fluid volume. J Clin Periodontol 2000;27:481-8.  Back to cited text no. 10
    
11.Boutros SM, Michalowicz BS, Smith QT, Aeppli DM. Crevicular Fluid enzymes from endosseous dental implants and natural Teeth. Int J Oral Maxillofac Implants 1996;11:322-30.  Back to cited text no. 11
    
12.Kaklamanos EG, Tsalikis L. A review on peri-implant crevicular Fluid assays potential in monitoring and predicting periimplant Tissue responses. J Int Acad Periodontol 2002;4:49-59.  Back to cited text no. 12
    
13.Lang NP, Wilson TG, Corbet EF. Biological complications with Dental implants: Their prevention, diagnosis and treatment. Clin Oral Implants Res 2000;11 (suppl 1):146-55.  Back to cited text no. 13
    
14.Fiorellini JP, Nevins ML, Sekler J, Chung A, Oringer RJ. Correlation Of peri-implant health and aspartate aminotransferase Levels: A cross-sectional clinical study. Int J Oral Maxillofac Implants 2000;15:500-4.  Back to cited text no. 14
    
15.Liskmann S, Zilmer M, Vihalemm T, Salum O, Fischer K. Correlation of peri-implant health and myeloperoxidase levels: A Cross-sectional clinical study. Clin Oral Implants Res 2004;15:546-52.  Back to cited text no. 15
    
16.Tözüm TF, Turkyilmaz I, Yamalik N, Tümer C, Kilinç A, Kilinç K, et al. Analysis of the possible Impact of inflammation severity and early and delayed loading On nitric oxide metabolism around dental implants. Int J Oral Maxillofac Implants 2005;20:547-56.  Back to cited text no. 16
    
17.Yamalik N, Caglayan F, Kilinc K, Kilinc A, Tümer C. The importance Of data presentation regarding gingival crevicular fluid Myeloperoxidase and elastase-like activity in periodontal disease And health status. J Periodontol 2000;71:460-7.  Back to cited text no. 17
    
18.Tözüm TF, Yildirim A, Caglayan F, Dincel A, Bozkurt A. Serum And gingival crevicular fluid levels of ciprofloxacin in patients With periodontitis. J Am Dent Assoc 2004;135:1728-32.  Back to cited text no. 18
    
19.Huri CB, Yamalik N, Kilinc K, Kilinç A, Etikan I, Eratalay K. Analysis of the relationship Between the severity of periodontal destruction and proteoglycan Metabolism of gingiva and gingival crevicular flu. J Clin Periodontol 2003;30:961-8.  Back to cited text no. 19
    
20.Atici K, Yamalik N, Eratalay K, Etikan I. Analysis of gingival Crevicular fluid intracytoplasmic enzyme activity in patients With adult periodontitis and rapidly progressive periodontitis. A longitudinal study model with periodontal treatment. J Periodontol 1998;69:1155-63.  Back to cited text no. 20
    
21.Eley BM, Cox SW. Cathepsin B/L-, elastase-, tryptase-, trypsinand Dipeptidyl peptidase IV-like activities in gingival crevicular Fluid: Correlation with clinical parameters in untreated Chronic periodontitis patients. J Periodontal Res 1992;27:62-9.  Back to cited text no. 21
    
22.Albandar JM, Kingman A, Lamster IB. Crevicular fluid level of Beta-glucuronidase in relation to clinical periodontal parameters And putative periodontal pathogens in early-onset periodontitis. J Clin Periodontol 1998;25:630-9.  Back to cited text no. 22
    
23.Wolff LF, Smith QT, Snyder WK, Bedrick JA, Liljemark WF, Aeppli DA, et al. Relationship between lactate Dehydrogenase and myeloperoxidase levels in human Gingival crevicular fluid and clinical and microbial measurements. J Clin Periodontol 1988;15:110-5.  Back to cited text no. 23
    
24.Kendall HK, Marshall RI, Bartold PM. Nitric oxide and tissue Destruction. Oral Dis 2001;7:2-10.  Back to cited text no. 24
    
25.Brennan PA, Thomas GJ, Langdon JD. The role of nitric oxide in Oral diseases. Arch Oral Biol 2003;48:93-100.  Back to cited text no. 25
    
26.Van't Hof RJ, Ralston S. Nitric oxide and bone. Immunology 2001;103:255-61.  Back to cited text no. 26
    
27.Hirose M, Ishihara K, Saito A, Nakagawa T, Yamada S, Okuda K. Expression of cytokines and Inducible nitric oxide synthase in inflamed gingival tissue. J Periodontol 2001;72:590-7.  Back to cited text no. 27
    
28.Lappin DF, Kjeldsen M, Sander L, Kinane DF. Inducible nitric Oxide synthase expression in periodontitis. J Periodontal Res 2000;35:369-73.  Back to cited text no. 28
    
29.29 Daghigh F, Borghaei RC, Thornton RD, Bee JH. Human gingival Fibroblasts produce nitric oxide in response to proinflammatory Cytokines. J Periodontol 2002;73:392-400.  Back to cited text no. 29
    
30.Shibata K, Warbington ML, Gordon BJ, Kurihara H, Van Dyke TE. Nitric oxide synthase activity in neutrophils from patients With localized aggressive periodontitis. J Periodontol 2001;72:1052-58.  Back to cited text no. 30
    
31.Aurer A, Aleksic J, Ivic-Kardum M, Aurer J, Culo F. Nitric oxide Synthesis is decreased in periodontitis. J Clin Periodontol 2001;28:565-8.  Back to cited text no. 31
    
32.Lamster IB, Oshrain RL, Fiorello LA, Celenti RS, Gordon JM. A Comparison of 4 methods of data presentation for lysosomal Enzyme activity in gingival crevicular fluid. J Clin Periodontol 1988;15:347-52.  Back to cited text no. 32
    
33.Johnson DL, Mcallister TN, Frangos JA. Fluid flow stimulates rapid and continuous release of nitric oxide in osteoblasts. Am J Physiol 1996;271: E205-8.  Back to cited text no. 33
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
   Introduction
    Materials and Me...
   Results
   Discussion
   Conclusions
    References
    Article Tables

 Article Access Statistics
    Viewed4179    
    Printed212    
    Emailed2    
    PDF Downloaded596    
    Comments [Add]    

Recommend this journal