Estimation and Correlation of Serum Albumin and Serum Alkaline Phosphatase Levels Between Smokers and Non-smokers With Generalized Chronic Periodontitis.

Background Periodontal disease is a chronic low-grade inflammatory disease triggered by periodontal microbial interaction present in the dysbiotic biofilm and the host's immune response further leads to the destruction of the supporting periodontal apparatus, which may, in turn, lead to tooth loss. Smoking is an environmental risk factor for periodontitis, and it enhances the secretion of various enzymes from host cells, which results in the initiation and progression of periodontal disease. The albumin concentration is related to nutrition and inflammation. Alkaline phosphatase (ALP), an enzyme found in various cells of the periodontium, is considered to cause the destruction of the periodontium. The study aimed to compare the serum albumin and serum ALP levels in smokers and non-smokers with generalized chronic periodontitis. Materials and methods The cross-sectional study included a total of 60 subjects. Subjects were divided into two groups, which included non-smokers with generalized chronic periodontitis (NS+P) and smokers with generalized chronic periodontitis (S+P). Clinical parameters analyzed were plaque index, gingival index, probing pocket depth, and clinical attachment level. The serum ALP and albumin levels were analyzed using a fully automated analyzer. Results The serum ALP levels were higher in the S+P group compared to the NS+P group. Conversely, the serum albumin levels were lower in the S+P group compared to the NS+P group. Conclusion There was a significant correlation of increased serum ALP levels and decreased serum albumin levels in the S+P group compared to the NS+P group.

The Association between Inflammatory Bowel Disease and Periodontal Conditions: Is There a Common Bacterial Etiology?

INTRODUCTION: The gastrointestinal system is strongly associated with the oral mucosa including periodontal tissues. Infl ammatory bowel disease (IBD) has two common forms: Crohn's disease (CD) and ulcerative colitis (UC). Local inflammation in periodontal diseases (PD) has an impact on infl ammatory diseases in various parts of the body. The existence of periodontitis in IBD patients suggests the possibility that the two inflammatory conditions may have common pathogenic pathways. Both diseases are multifactorial conditions in which genetic and environmental factors initiate and maintain the chronic inflammatory response. AIM: The aim of this review was to determine the current state of understanding of the characteristics and mechanisms underlying the association between IBD and periodontal diseases, with emphasis on the role of microorganisms. METHODS: A computer-assisted MEDLINE search was performed to find the relevant articles concerning IBD and periodontal diseases published until September 2016. RESULTS AND CONCLUSION: A number of studies have showed an association between PD and IBD. Both diseases share genetic and environmental etiological factors. The precise role of intestinal bacteria remains vague. The periodontal microbiota that might be involved in the association of these diseases are Fusobacterium nucleatum, Campylobacter rectus and Campylobacter concisus. Fungal and viral microbiota dysbiosis should also be evaluated as common pathogenic pathways in IBD and periodontal disease.

Osteopontin attenuation of dextran sulfate sodium-induced colitis in mice.

Osteopontin (OPN) is a matricellular cytokine present in most tissues and body fluids; it is known to modulate immune responses. In previous studies using the dextran sulfate sodium (DSS) acute colitis model, we found exacerbated tissue destruction and reduced repair in OPN-null ((-/-)) mice compared with wild-type (WT) controls. As OPN is normally present in milk, we hypothesized that administration of OPN may protect the intestines from the adverse effects of experimental colitis. A volume of 20 or 2 microg/ml bovine milk OPN, dissolved in drinking water, was given to mice 24 h before, and during administration of DSS. Clinical parameters of colitis and neutrophil functions were analyzed as previously reported. Orally administered OPN was absorbed and detected in the colon mucosa by immunohistochemistry. The 20 microg/ml OPN- and DSS-treated WT mice showed 37% less weight loss and reduced colon shortening and spleen enlargements than control mice (P<0.05). OPN administration also reduced the disease activity index, improved red blood cell counts, and reduced gut neutrophil activity compared with the DSS-treated WT mice that were not administered OPN (P<0.05). Immunohistochemical detection of F4/80-labelled cells (macrophages) was also less frequent. The level of transforming growth factor beta1 (TGF-beta1) was increased and the levels of pro-inflammatory mediators decreased in colon tissue samples of OPN-treated mice analyzed by ELISA. The reversal of experimental colitis parameters by exogenous OPN was not as robust in the OPN(-/-) mice. Administration of prokaryotic-expressed recombinant OPN and bovine serum albumin were ineffective. This study shows that administration of a physiological concentration of milk OPN in drinking water ameliorates the destructive host response in DSS-induced acute colitis.

Role of osteopontin in neutrophil function.

Osteopontin (OPN) is important for the function of fibroblasts, macrophages and lymphocytes during inflammation and wound healing. In recent studies of experimental colitis we demonstrated exacerbated tissue destruction in OPN-null mice, associated with reduced tumour necrosis factor-alpha expression and increased myeloperoxidase activity. The objective of this investigation therefore was to determine the importance of OPN expression in neutrophil function. Although, in contrast to macrophages, neutrophils expressed low levels of OPN with little or no association with the CD44 receptor, intraperitoneal recruitment of neutrophils in OPN-null mice was impaired in response to sodium periodate. The importance of exogenous OPN for neutrophil recruitment was demonstrated by a robust increase in peritoneal infiltration of PMNs in response to injections of native or recombinant OPN. In vitro, OPN(-/-) neutrophils exhibited reduced chemokinesis and chemotaxis towards N-formyl methionyl leucyl phenylalanine (fMLP), reflecting a reduction in migration speed and polarization. Exogenous OPN, which was chemotactic for the neutrophils, rescued the defects in polarization and migration speed of the OPN(-/-) neutrophils. In contrast, the defensive and cytocidal activities of OPN(-/-) neutrophils, measured by assays for phagocytosis, generation of reactive oxygen species, cytokine production and matrix metalloproteinase-9, were not impaired. These studies demonstrate that, while exogenous OPN may be important for the recruitment and migration of neutrophils, expression of OPN by neutrophils is not required for their destructive capabilities.

Exacerbated tissue destruction in DSS-induced acute colitis of OPN-null mice is associated with downregulation of TNF-alpha expression and non-programmed cell death.

Osteopontin (OPN), a pro-inflammatory mediator, is constitutively expressed in normal gut and is upregulated in inflammatory colitis. To determine the significance of OPN in inflammatory bowel disease, we studied the development of acute, experimental colitis induced by dextran sulfate sodium (DSS) in OPN-null and wild-type (WT) mice. OPN expression was markedly increased in WT diseased colons, while a higher disease activity index, including spleen enlargement, bowel shortening, and mucosal destruction, was observed in OPN-null mice. Although peripheral blood neutrophil numbers were lower in DSS-treated OPN-null mice, tissue myeloperoxidase levels, reflecting enhanced neutrophil activity, were increased in the diseased colons. In comparison, lymphocyte numbers in peripheral blood were increased earlier than in DSS-treated WT mice. Despite a significantly greater spleen enlargement, flow cytometric analysis of splenocytes from the DSS-treated OPN-null mice revealed lower numbers of differentiated macrophages and (CD4+ and CD8alpha+) lymphocytes. Whereas pro-inflammatory cytokines, including G-CSF, RANTES, MIP1alpha, and TNF-alpha, were increased < 10-fold in DSS-treated WT splenocytes, expression of these cytokines was dramatically suppressed in the DSS-treated OPN-null splenocytes as well as gut tissues. The suppressed TNF-alpha response in OPN-null mice was reflected in a marked increase in non-apoptotic cell death in diseased colons. Collectively, these studies demonstrate that OPN is required for mucosal protection in acute inflammatory colitis.