Journal of Patient Care is a peer-reviewed Nursing journal that focuses on a wide range of topics in this field such as patient health, patient safety, patient education, and so on. It provides a platform for authors to contribute to the journal and the editorial office promises a peer review process for submitted manuscripts to ensure the quality of publication.

This journal, which ranks among the best open access journals, aims to publish the most thorough and trustworthy source of information on discoveries and current developments in the form of original articles, review articles, case reports, short communications, etc.

Osteoarthritis (OA) is a form of degenerative joint disease caused by the degradation of joint cartilage and underlying bone that affects one out of every seven persons in the United States. It is thought to be the world's fourth greatest cause of disability. Joint pain and stiffness are the most prevalent symptoms. Symptoms usually worsen slowly over time. They may appear just after activity at first, but they might become continuous with time.  Other symptoms may include joint swelling, restricted range of motion, and weakness or numbness of the arms and legs if the back is involved. The two joints near the ends of the fingers and the joint at the base of the thumbs are the most usually affected, followed by the knee and hip joints, and the neck and lower back joints.

  One side of the body's joints are frequently more impacted than the other.  Symptoms might disrupt employment and routine daily activities. Unlike certain other varieties of arthritis, this one affects only the joints and not the internal organs. Inherited factors, aberrant joint or limb development, and prior joint injuries are among the causes. Overweight people, those with different-length legs, and people who work in occupations that put a lot of strain on their joints are at higher risk.  The mechanical stress on the joint and low-grade inflammatory processes are thought to be the primary causes of osteoarthritis. It grows as the underlying bone deteriorates and cartilage is removed. Muscle atrophy may take place when discomfort makes it difficult to exercise. Signs and symptoms are often the basis for diagnosis, with imaging studies and other testing required to confirm or rule out other conditions. Osteoarthritis does not cause hot or red joints like rheumatoid arthritis does. Lubrication of cartilage inside synovial joints involves a complex interplay of numerous mechanical and molecular variables, resulting in reduced friction between opposing articular cartilage surfaces. A layer of lubricating molecules covers the surfaces of articular cartilage and functions as a border lubricant in healthy weight-bearing joints, resulting in almost frictionless joint motion.

Lubricant components of synovial fluid (SF), such as hyaluronic acid or hyaluronan (HA), lubricin, and surface-active phospholipids, interact with and adsorb to the surface of articular cartilage and have been hypothesised to increase boundary lubrication. Alterations in the content and concentration of these molecules result in inadequate border lubrication and may be linked to degenerative joint illnesses like osteoarthritis (OA). HA is an extracellular matrix component found in SF, cartilage, eye fluid, vitreous humour, and tissues such as the lung, kidney, brain, and muscle. In human SF, this glycosaminoglycan has a wide molecular weight (MW) variation, ranging from 27 kDa to 10 MDa. HA creates long nonsulfated chains of repeating disaccharides, including D-glucuronic acid and N-acetylD-glucosamine, and is responsible for the high viscosity of SF. HA has been linked to a variety of activities, including tissue hydration, lubrication, and interactions with extracellular matrix proteins and proteoglycans. Furthermore, HA interacts to the cell surface receptors CD44 and RHAMM, which influence signalling pathways in inflammation, cell and tissue functions, and the development of catabolic enzymes including aggrecanases. In animal studies, HA in the MW range of 0.5-1.0 x 10(6) Da partly recovers SF rheological characteristics and fibroblast-like synoviocytes (FLSs) metabolism. High-MW HA suppresses phospholipase A2 activity, hence preserving phospholipid integrity. Notably, due to enzymatic breakage of HA chains, HA in SF from 24 human knee joints with advanced OA was observed to be moved toward the low-MW forms. In contrast, the MW distribution of HA in SF from 5 patients with advanced OA remained unaffected compared to 5 patients having meniscectomy or ligament repair without any obvious OA. Human OA SF HA concentrations have been observed to be normal, but decline in RA. Although the exact role of HA to total cartilage border lubrication is still being debated, viscosupplementation with intra-articular HA is still often utilised to treat OA. Lubricin is a large mucin-like glycoprotein with three domains: an N-terminal cysteine-rich somatomedin B-like domain, an O-linked oligosaccharide-rich domain, and a C-terminal domain. PRG4 encodes lubricin homologs such as the superficial zone protein, proteoglycan 4 (PRG4), megakaryocyte-stimulating factor precursor, and arthritis-like camptodactyly-arthropathy-coxavara-pericarditis syndrome protein. Lubricin is generated and released by chondrocytes from the superficial zone of articular cartilage, FLSs, and cells in the meniscus, and it is present in SF, where it works as a cartilage border lubricant either alone or in conjunction with HA. Lubricin is expressed in human SF in many isoforms, the one that offers the best border lubrication being unknown. SF from human knee joints with advanced OA was shown to have much higher lubricin concentrations than normal human SF, as well as a similar friction-lowering lubricating effect. However, lubricin levels in certain OA SF can be low relative to normal, which is associated with a decreased cartilage border lubricating function. It has been hypothesised that lubricin is chondroprotective, perhaps shielding articular chondrocytes against apoptosis