Commentary - Archives of General Internal Medicine (2021) Volume 5, Issue 10

Brief note on arthritis

Sarah David Shah^*

Department of Cognitive Neuroscience, University of West Florida, Pensacola, United States of America

Corresponding Author:

Sarah David Shah
Department of Cognitive Neuroscience
University of West Florida
Pensacola
United States of America
E-mail: David_sa_@shah.edu

Accepted date: November 22, 2021

Citation: Shah SD. Brief note on arthritis. Arch Gen Intern Med 2021;5(10):10.

Description

Arthritis is an inflammation caused in joints; a regular kind of arthritis is Osteoarthritis. Other common rheumatic conditions associated with arthritis include gout, fibromyalgia, and Rheumatoid Arthritis (RA). Pain, soreness, stiffness, and swelling in and around one or more joints are common symptoms of rheumatic disorders. The signs and symptoms may appear gradually or suddenly. The immune system and numerous internal organs of the body might be affected by certain rheumatic disorders. Several extensive symptoms are caused by Rheumatoid Arthritis which affects body organs.

According to the studies, pain impulses originating in arthritic joints, in addition to the metabolic processing of those signals as they reach the spinal cord, aggravate and expand arthritis. Furthermore, researchers discovered that, neural pathways conveying pain signals transmit inflammation from arthritic joints to the spine and back, resulting in illness on both ends.

Technically, pain is a patient's conscious awareness of discomfort. First, information must be transferred from the dorsal horns of the spinal cord's pain processing centers to the injured knee via nerve cell routes, a process known as nociception. New research analysis recommends that two-way nociceptive "crosstalk" may allow joint arthritis to spread inflammation into the spinal cord and brain and then spread across the Central Nervous System (CNS) from one joint to another.

Furthermore, if joint arthritis may generate neuroinflammation, it may have a role in diseases such as alzheimer's, dementia, and multiple sclerosis. Researchers have found potential therapeutic targets that might interfere with critical inflammatory receptors on sensory nerve cells as a novel strategy to treat Osteoarthritis (OA), which affects 21 million people across the world and degrades joint cartilage. OA is the most prevalent type of arthritis, and it creates deformities and constant pain when the protective cushion between bones in weight-bearing joints like the knees and hips wears away.

However, recent research has indicated that few biochemical changes play a crucial role. The experiments revealed that, increasing Interleukin-1 in a peripheral joint will promote the production of Interleukin-1 in the dorsal horns of the spinal cord. The increasing Interleukin-1 levels in astrocytes in the spinal cord induced more osteoarthritic symptoms in the joints.

The previous study has shown that, specific brain pathways from which pain signals travel become more sensitive and cause inflammation. The same molecules that produce inflammation also produce hypersensitive reactions. Previous research has demonstrated that astrocytes, non-nerve cells in the Central Nervous System that maintain the spinal cord and brain, function as immune cells of CNS organs.

When activated, they produce cytokines such as Interleukin-1 to combat illness. The same cytokines produced by CNS glia may also be released by neurons in joints, explaining how pain, inflammation, and hypersensitivity are transmitted.

The Calcitonin Gene-Related Peptide is one of the inflammatory agents (CGRP). The researchers discovered more levels of Calcitonin Gene-Related Peptide (CGRP) synthesis in primary sensory fibers in the same areas as interleukin-1 levels increased, suggesting that, interleukin-1 released by sensory neurons may promote CGRP release in joints. Previous research has shown that, CGRP can induce cartilage-producing cells such as chondrocytes to mature too fast and die, which is a characteristic of Osteoarthritis.

As discussed, the increasing interleukin-1 from the joints can go through sensory nerve pathways to the spinal cord, causing inflammation and that higher interleukin-1 inflammatory in the spine is enough to cause Osteoarthritis in peripheral joints. However research reveals that, few biochemical studies in the signal pathway can reduce the production of interleukin-1. By reducing the production of interleukin-1, inflammation can be reduced. Arthritis is an autoimmune disorder which causes severe pain but there is no particular therapy for preventing it.