Vitamin D attenuates inflammation, fatty infiltration, and cartilage loss in the knee of hyperlipidemic microswine.
Osteoarthritis (OA) of the knee joint is a degenerative process resulting in cartilage loss. Recent evidence suggests that OA is not merely a disease of cartilage but a disease of the entire knee joint and that inflammation may play an important role. OA has been associated with vitamin D deficiency. Vitamin D as an immunomodulator and anti-inflammatory agent may attenuate inflammation in the knee. The aim of this study was to assess the anti-inflammatory effect of vitamin D on inflammation in the knee.



This study was conducted with 13 microswine on a high cholesterol diet categorized into three groups of vitamin D-deficient, vitamin D-sufficient, and vitamin D supplementation. After 1 year, microswine were killed, and their knee joint tissues were harvested. Histological and immunofluorescence studies were carried out on the tissue specimens to evaluate the effect of vitamin D status.



Histological and immunofluorescence studies of the knee joint tissues showed (1) increased inflammation in the knee joint tissues, (2) fatty infiltration in quadriceps muscle, patellar tendon, and collateral ligaments, and (3) chondrocyte clustering in the vitamin D-deficient and vitamin D-sufficient groups compared with the vitamin D supplementation group. Architectural distortion of the quadriceps muscle, patellar tendon, and collateral ligaments was also seen in the areas of inflammatory foci and fatty infiltration in the vitamin D-deficient group.



Decreased inflammation and fatty infiltration in the vitamin D supplementation group suggest the potential role of vitamin D in attenuating inflammation and fatty infiltration as well as in protecting the architecture of the tissue in the knee joint.
Department of Clinical and Translational Science, Creighton University School of Medicine, CRISS II Room 510, 2500 California Plaza, Omaha, NE, 68178, USA.
Vikrant
V
Rai
Department of Pathology, Creighton University School of Medicine, 601 North 30th Street, Omaha, NE, 68131, USA.
Nicholas E
NE
Dietz
Department of Orthopedic Surgery, Creighton University School of Medicine, Omaha, NE, 68178, USA.|CHI Health Alegent Creighton Clinic, 601 North 30th Street, Suite 2300, Omaha, NE, 68131, USA.
Matthew F
MF
Dilisio
Department of Clinical and Translational Science, Creighton University School of Medicine, CRISS II Room 510, 2500 California Plaza, Omaha, NE, 68178, USA.
Mohamed M
MM
Radwan
Department of Clinical and Translational Science, Creighton University School of Medicine, CRISS II Room 510, 2500 California Plaza, Omaha, NE, 68178, USA. dkagr@creighton.edu.
Devendra K
DK
Agrawal
D000273:Adipose Tissue / Q000473:pathology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002358:Cartilage, Articular / Q000187:drug effects / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D005455:Fluorescent Antibody Technique; D006949:Hyperlipidemias; D007249:Inflammation / Q000473:pathology*; D007719:Knee Joint / Q000187:drug effects* / Q000473:pathology; D020370:Osteoarthritis, Knee / Q000473:pathology*; D052097:Quadriceps Muscle / Q000473:pathology; D013552:Swine; D014807:Vitamin D / Q000494:pharmacology*
D000893:Anti-Inflammatory Agents; D014807:Vitamin D
Cartilage loss; Fatty infiltration; Inflammation; Inflammation attenuation; Osteoarthritis; Vitamin D deficiency; Vitamin D supplementation