How does Lichen Planus think?
The cause of Lichen Planus is still unclear, and several factors may contribute to its progression. Hepatitis C, certain drugs like antimalarials, NSAIDs, metals, and contact with allergens are some examples. When it comes to Lichen Planus, the first question that should come to mind is what's going on internally. The health of our skin reflects the health of our internal organs. The integrity and function of both the gut and the skin need to be assessed when dealing with skin conditions like Lichen Planus. There has been a variety of activities and behavioral patterns reported in connection with Lichen Planus. How does Lichen Planus think?
Science indicates that Lichen Planus confuses an individual's immune system by altering their self-cell configuration. In this case, it is referred to as a T-cell-mediated autoimmune disorder. What does this even mean?
Under Normal Condition
Self-cells are members of your immune system that protect you from viruses and bacteria. The immune system recognizes non-self-cells as unwelcome visitors because they possess antigens, which are proteins along their bodies. In response, macrophages, cytokines, lymph nodes, lymphocytes, and T and B cells are released by the immune system.
Several events occur when an immune response is triggered. A macrophage is a white blood cell that swallows and eliminates its advisory that are in close proximity, much like how a goldfish consumes its food. As a way of signaling to other cells that an invader is present, macrophages take DNA samples from non-self-cells and spread them throughout the body.
When these white blood cells eliminate their opponent, they release inflammatory substances called cytokines. Think of these as encrypted messages. This is the way macrophages communicate. These encoded messages are packaged in distinctive shapes that fit perfectly into other macrophage receptors, like mailboxes. Essentially, the cytokines provide the other macrophages with a Most Wanted flyer of the intruder. By doing this, it will make it easier to detect the intruder if it resurfaces within the body. This avoids the need to deploy the immune response team in masses.
Lymph nodes, which serve as the immune system's information hub, are the go-to location for macrophages when outnumbered. Throughout the human body, these centers are abundant. Basically, lymphocytes serve as receptionists for lymph nodes, and macrophages let them know when they should respond. B-cells and T-cells are the two kinds of lymphocytes, which multiply and help macrophages. DNA samples originally collected by macrophages are scattered throughout the body to help the T-cells identify and form customized messages against these intruders. In response, T-cells divide, increase in number, and prepare for combat. They work in conjunction with macrophages to eliminate unwelcome visitors out of the body. Likewise, B-cells produce more cytokines that are delivered to macrophages as they grow in number. Inflammatory cytokines are released during immune responses, causing swelling and redness.
Autoimmune Condition
The immune cells of people with autoimmune conditions mistake their own cells for invaders. In this situation, the immune system is continually responding, which causes it to become overworked. It is common knowledge in the medical community that chronic inflammation damages healthy cells and layers.
Lichen Planus
In Lichen Planus, the immune system perceives self-cells within basal keratinocytes as enemies, activating T-cells to attack and destroy them. Keratinocytes are crucial for maintaining skin health since they promote skin thickness and produce vitamin D. People with this condition tend to have low levels of vitamin D. It is highly likely that normal regulatory features such as the release of antimicrobial properties, the pH of the skin, and the communication between healthy microbes and the immune system are operating at optimal level.
The stratum corneum and stratum granulosum of Lichen Planus individuals tend to be thicker and stiffer. These layers are inhibited from functioning normally as a result. The stratum granulosum houses keratinocytes that produce keratin, while the llamellar granules keep cells intact with their lipid attributes. In the meantime, the stratum corneum protects the skin from intruders. It also makes use of UVB from sunlight in order to manufacture vitamin D. It is essential for proper skin health to maintain healthy antioxidant and nutrient reserves. However, an overstimulated immune system drains these reserves. This encourages opportunistic bacteria and viruses to redesign the environment of the skin to help them set up shop, causing further havoc. It involves changing the pH of the skin, utilizing the natural lipids inside and around it as they mature, and removing the moisture that is naturally present.
Researchers have noticed a white band of lymphocytes around the dermo-epidermal junction which is a sign the immune system is fighting to eliminate a perceived threat by mobilizing various immune response substances in people with Lichen Planus. The presence of the white band is problematic. This is similar to construction work happening on Interstate 95, which slows down traffic. The lymphocytes are the construction workers. A job that becomes labor-intensive or time-consuming affects the skin's integrity because nutrients can't reach their destination in a timely manner.
Scientists and clinicians have yet to determine whether dermatological or gastrointestinal complications are the primary culprit to this condition, or whether both occur simultaneously. Poor nutrition exacerbates skin issues. Those suffering from Lichen Planus might benefit from nutritional and dietary supplements along with their steroid cream, or without it. For guidance, it is prudent to consult a GP or integrative practitioner. Our next script, Let my Script Parley, will focus on nutritional and dietary supplement recommendations for Lichen Planus. Until next time, Stay Strong & Stay Vivid.
Reference
1. Arnold DL. & Krishnamurthy K. (2022). Lichen Planus. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK526126/?report=reader#_NBK526126_pubdet_.
El-Shebiny. E.M. et al. (2021). Bridging autoinflammatory and autoimmune diseases. The Egyptian Journal of Internal Medicine. https://doi.org/10.1186/s43162-021-00040-5.