Osteoarthritis (OA) is most prevalent joint disease and major contributor to non-fatal burden in India, with prevalence rates of 22% - 39%. The use of conventional medication can be associated with insufficient clinical management and serious side effects. The present study aims to evaluate the anti-arthritic activity and chondrocytes protection and regeneration potential of Joint Support Product (JSP) in monosodium Iodoacetate induced Osteoarthritis rat model. Pain threshold, knee joint swelling, Blood inflammatory parameters like Tissue necrosis factor, Interlukin-6, Leukotriene B 4, C- reactive protein and arthritic biomarkers Matrix metalloproteinase-13 and Cartilage Oligomeric Matrix Protein, were estimated. Also Radiographic and histopathological evaluation were done to estimate the severity of OA. Treatment of JSP demonstrated significant increase in pain threshold by 68 % and decrease in knee joint swelling by 92 %. The inflammatory markers decreased significantly (p< .00001) after treatment with JSP. The Tissue necrosis factor decreased by 55 %, Interlukin-6 by 61%, Leukotriene B 4 by 57%, C- reactive protein by 69 % and arthritic biomarkers - Matrix metalloproteinase by 88% and Cartilage Oligomeric Matrix Protein by 37% as compared to disease control rats. Also the radiological evaluation and gross histopathology of rats showed improved chondrocytes structure. Thus JSP’s analgesic, anti-inflammatory, chondrocyte regeneration, and chondroprotective properties have therefore demonstrated an anti-arthritic impact.

Inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis (UC), are chronic conditions in which idiopathic inflammation of the gastrointestinal tract wall is the characteristic feature.
The etiology of these disorders is not fully elucidated, proposed causes including environmental, immunological and genetic factors. A consensus hypothesis is that in genetically susceptible individuals, both exogenous factors (eg. Intestinal flora) and factors related to the host (barrier function of epithelial cells, innate and acquired immune response function) produce a chronic immune dysfunction in the intestinal mucosa which is further modified by the action of environmental factors (eg. smoking).

Inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis (UC), are chronic, idiopathic diseases characterized by the inflamation of the wall tube (1). Ulcerative colitis was first described in the mid-1800s (2), whereas Crohn's disease was first reported later, in 1932, as "regional ileitis" (3). Because Crohn's disease can involve the colon and shares clinical manifestations with ulcerative colitis, these entities have often been conflated and diagnosed as inflammatory bowel disease, although they are clearly distinct physiopathological entities. Ulcerative colitis is the most common form of inflammatory bowel disease worldwide. In contrast to Crohn's disease that can extend in the entire intestinal wall, ulcerative colitis is a disease of the mucosa that is less prone to complications and can be cured by means of colectomy, and in many patients, its course is mild (4).
Until recently, it was considered that, unlike Crohn's disease (whose location can be at any level of the digestive tract), ulcerative colitis is strictly localized in the colon. However, in the recent years, increasingly more studies reveal the existence of a moderate, chronic, diffuse gastroduodenitis in pacient with ulcerative colitis, which normally causes no macroscopical lesions being highlighted only based on histopathologic examination (5). Most of these studies invoke the presence in the duodenum of a diffuse inflamation with neutrophilic infiltration in the glandular crypts, with redness and swelling during an acute exacerbation. In the stomach the predominant lesions are chronic focal gastritis (5,6,7).