Jasdeep Kaur1 , Balwant Rai2
1. Model Town , Kapurtala, Panj ab , India.
2. Editor In Chief International Journal of Dental science, Ex-lecturer P.D.M. Dental College and Research Institute, Haryana, India.
Corresponding author: “Dr.Jasdeep Kaur” jasdeep.kor @gmail.com
J Pak DentAssoc.2009; 18(1): 023 – 024.
Periodontitis is usually a painless, slowly progressing infectious disease in tooth supporting tissues. The main etiological agents in periodontitis are dental plaque bacteria, especially gram negative micro organisms. The objective of the present study was to evaluate whether the salivary TNF-alpha concentration affect the periodontitis.
Salivary tumor necrosis factor alpha levels were estimated in 25 patients with periodontitis and ten healthy normal. Concentrations of TNF-alpha were determined using the human TNF-alpha ELISA kit (SIGMA ImmunoChemicals St Louis, MO, USA).
Significantly higher levels of Salivary tumor necrosis factor alpha were observed in periodontitis patients as compared to controls (p<0.001). Saliva provides an ideal medium for the detection of pro-inflammatory markers of the oral cavity.
Salivary TNF-alpha analysis may be a useful diagnostic tool and a potential prognostic marker in periodontal disease.
Periodontal disease, salivary levels, tumour necrosis factor-alpha
Periodontal inflammation results in gingival bleeding, pocket formation, destruction of alveolar bone, and eventually loss of teeth. The gingival bleeding is a clinical system of both scurvy and periodontitis, the two conditions are distinct disease entities. Unlike for scurvy, which is caused by vitamin C deficiency, the etiological agents in periodontitis are dental plaque bacteria, especially gram negative microorganisms. The continued local or systemic bacterial stimulus causes release of proinflammatory mediators, which may have a role in the pathogenesis of atherosclerosis and stroke.” Lower vitaminosis is associated primarily with defective collagen synthesis, causing tissue dysfunction such as impaired wound healing and ruptured capillaries because of insufficient support of the capillary walls by the connective tissues.3 The objective of this study is to present data characterizing the pattern of TNF-alpha production in whole saliva of patients with periodontitis, and to evaluate whether the salivary concentrations of TNF-alpha were changed in periodontitis
Twenty five patients (M: F, 13:12) age group 17-30 years having at least 6 mm loss of clinical attachment who had been referred to our clinic were selected for the study due to their severe periodontitis and were undergoing treatment for this condition. Clinical periodontal examination was performed on all the patients and controls by two calibrated examiners using a calibrated periodontal probe (Hu-friedy, Chicago, IL, USA). The following variables were determined: oral hygiene status, gingival inflammation, probing depth, and clinical attachment level measurements. Oral hygiene status was assessed as the percentage of surface demonstrating plaque. Probing depth and attachment level measurements were performed at six sites on each tooth. Gingival bleeding was assessed on the sites at which probing depth was measured. Gingival redness was determined on two gingival units per tooth. After informant consent had been obtained, each individual expectorated 10 ml of unstimulated whole saliva into a sterile centrifuge tube. The saliva was centrifuged for 3 min at 8000/g and the clarified supernatant was filtered through a 0.45 mm low protein binding membrane, separated into 0.5 ml aliquots
and frozen at _808C until use. Concentrations of TNF-a were determined using the human TNF-a ELISA kit (SIGMA ImmunoChemicals St Louis, MO, USA).4 The assay was performed according to the manufacturer’s instructions, and the results are expressed in pg/ml. The detection limit for TNF-a was 4.4 pg/ml, respectively. Data were analylased by SPSS 11.0 version and Students’ t test were applied.
Sufficient quantities of TNF-a (1.45 pg/ml)were present in all saliva sample obtained from healthy subjects. Salivary levels of TNF-a were elevated in all patients presenting symptomatic periodontitis. The median values (2.83 pg/ml)) of TNF-a in saliva of the patients with the periodontitis, were significantly (p<0.001) higher in comparison with the values obtained from control subjects.
We found a significantly higher amount of TNF-a in all saliva samples obtained from patients with periodontitis in comparison with the healthy controls. A permanent or prolonged presence of high TNF-alpha amounts in saliva may contribute to progression of periodontitis.” As a diagnostic fluid, saliva is underused.
It offers distinctive advantages over serum because it can be collected non-invasively by individuals with modest training. Further more, saliva analysis demonstrated comparable values of various biochemical and immunological parameters with those that are routinely evaluated in blood.6 Saliva has more diagnostic value that is generally appreciated and has a role as an aid in the diagnosis of systemic and especially oral pathologies. Our data suggest an important role of high concentrations of TNF-alpha in perpetuation of the pathogenetical events in periodontitis. Inhibiting TNF-alpha activities in this disease may provide therapeutic benefits but more experimental and clinical studies are required for possible efficacy of drugs that can interfere with excess TNFalpha”.
Based on the presence of TNF-alpha in whole saliva we think that saliva analysis is a useful, worthwhile tool in the diagnosis and follow-up of periodontal disease, particularly in patients with gingivitis and periodontitis affections of oral mucosa.
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