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The skin care industry is fast approaching a watershed moment in the treatment of aging skin. Increasingly, scientific evidence suggests that many of today’s trademark treatments may actually exacerbate the conditions they’re designed to treat in the long term, thanks to a phenomenon known as inflammaging. This previously unknown consequence poses a challenge to product developers who must adapt their formulations to meet shifting consumer demands or risk losing their shares of the market. As the concept of inflammaging goes mainstream, it may result in a widespread change in the professional skin care industry.
First coined by University of Bologna professor Claudio Franceschi, PhD, more than a decade ago, inflammaging began as a theory linking underlying inflammatory changes to the causes of most age-associated diseases. Since its inception, research continues to present convincing evidence taking this concept from theory to fact.1–3
The term “inflammaging” is used to describe the aging phenomenon induced by chronic, persistent inflammation. Most people are familiar with the visible inflammation that can be seen on the surface of the skin, with redness representing a sign of infection, irritation or discomfort. However, inflammation can also be invisible. All skin—and certainly weakened or aged skin—is subject to inflammation, even at low intensities. It is this underlying inflammation that ultimately exhausts the body’s defense system, dismantling key youth-sustaining skin structures, and resulting in collagen and elastin degradation, as well as a breakdown of the skin’s barrier function.
The inflammaging process involves a highly complex chain of events, by which acute inflammation gradually gives way to chronic, or silent, inflammation. To understand how to combat inflammaging, skin care professionals must first understand the inflammatory cascade of reactions that erode the skin’s structure, ultimately manifesting in the form of deep wrinkles, hyperpigmentation and flaccid, inelastic tissue.
Inflammation is the body’s response to cellular aggression or injury. It represents a defense mechanism designed to heal cells from injury and protect the body from the consequences of that injury. Cell injury may occur due to trauma, genetic defects, physical and chemical aggressions, tissue death, foreign bodies, immune reactions and infections. Inflammation also facilitates early tissue healing and repair, and allows the body to restore itself to a normal form and function.
Acute inflammation. It all starts with acute inflammation, which is characterized by rapid onset and short duration. Generally associated with redness, swelling, pain, warmth and loss of function, acute inflammation manifests with the oozing of fluid and plasma proteins, and the emigration of white blood cells, or leukocytes. Of the five types of leukocytes that the body produces, it is primarily the neutrophils that make an appearance during acute inflammation, producing the whitish-yellow pus characteristic in wounds.
Chronic inflammation. In contrast, chronic inflammation is of prolonged duration and manifests microscopically by the presence of two different categories of white blood cells, known as lymphocytes and macrophages. Lymphocytes function as “killer” cells, disabling and destroying infected tissue, such as tumors or infected cells, while macrophages literally consume cellular debris and pathogens. Together, these aggressive forms of white blood cells can result in the scarring of connective tissue and tissue death.
The healing of an injury is a complicated process. It starts as soon as the injury occurs and can take nine months or more to complete. There are three phases to the healing process: the inflammatory phase, the proliferation phase and the remodeling phase.
During the inflammatory phase, pro-inflammatory proteins enter damaged areas, causing swelling as tissues push apart. Following this, white blood cells, including macrophages, begin the proliferation stage by cleansing the wound and jump-starting the repair process. During this stage, the wound contracts and receives the oxygen and nutrients vital for regeneration. Lastly, the remodeling stage is characterized by the production, organization and remodeling of collagen to strengthen the wound.
However, even after the wound has healed, the resulting scar tissue is more vulnerable to injury and deformation than the original tissue. Science now shows that repeated injury leads to the chronic state of inflammation known as inflammaging.4
Today, the direct link between extrinsic skin aging and inflammation is well-established and documented. Elias and Feingold demonstrated the reciprocal effect of many chronic inflammatory diseases—such as psoriasis, and atopic and seborrheic dermatitis—on the stratum corneum barrier, which maintains healthy hydration levels in the skin.5,6
The integrity of this barrier is maintained by metabolic balance, such as the synthesis of collagen fibers, and the replacement of old and worn out fibers, by enzymes called matrix metalloproteinases (MMPs) and is regulated by tissue inhibitors of matrix metalloproteinases (TIMPs).
Inflammaging destroys this balance, decreasing cellular metabolic activity and collagen renewal. Externally, the skin loses its suppleness and elasticity, and becomes flaccid. It is also known that inflammaging generates reactive oxygen species (ROS), causing age-accelerating oxidative damage, which further perpetuates a chronic, pro-inflammatory state.7
Inflammaging can be prevented—and even reversed—by using a wide spectrum of topical products formulated with anti-inflammatory and antioxidant ingredients. In addition to inhibiting the key mediators of inflammation and aging processes, these ingredients should help reinforce, protect and boost the antioxidant response system.