It may sound like just another beauty buzzword, but ‘inflammaging’ has been quietly reshaping how scientists understand ageing for over two decades. First coined in 2000 by longevity scientist Claudio Franceschi, the term describes the chronic, low-grade inflammation that builds within the body over time—often without obvious symptoms—and is now recognised as a key driver behind many age-related diseases.
More recently, those same principles have been applied to the skin. Dermatologists now view inflammation not just as something that flares during breakouts or irritation, but as a constant, underlying process that can slowly erode collagen, disrupt the barrier and accelerate visible ageing. From pigmentation and sensitivity to loss of firmness and fine lines, inflammaging is increasingly seen as the quiet force at work beneath the surface.
So what does it actually mean for our skin—and how much control do we really have over it? We asked leading dermatologists to explain.
What is inflammaging—and is it really behind how our skin ages?
Inflammation isn’t the sole cause of ageing skin, but it plays a key role. As consultant dermatologist Dr Aiza Jamil explains, “Skin ageing can generally be divided into two categories; Intrinsic ageing (genetic, hormonal, chronological) and extrinsic ageing (UV, pollution, lifestyle). Inflammation doesn’t replace these key ageing factors, but rather amplifies and links them. It amplifies the factors already playing a part in skin ageing, which include DNA damage, oxidative stress, loss of stem cell function, and cellular senescence.”
Consultant dermatologist Dr Anjali Mahto agrees that inflammaging is one piece of a much bigger biological picture. “Inflammaging, which is essentially chronic, low-grade inflammation, is arguably a piece of the puzzle when it comes to visible ageing, but it isn’t the only piece. You have intrinsic ageing, the inevitable way in which your skin will age due to genetics, and while we would naturally age slowly over decades, inflammation from UV, stress and lifestyle can that process into overdrive.”
What does inflammaging actually do to the skin?
At a cellular level, inflammation is the skin’s immune system switching into defence mode—but when that response never fully turns off, damage accumulates slowly but surely.
Dr Jamil explains: “At a cellular level, skin inflammation is an immune response to injury or pathogens, with the activation of resident cells (keratinocytes, mast cells). This leads to the chronic release of cytokines (IL-1, IL-6, TNF-α), prostaglandins, matrix metalloproteinases (MMPs) and reactive oxygen species (ROS), which act like stress signals, causing damage to collagen, elastin, pigmentation and skin barrier health over time.”
Those stress signals also change how skin cells behave. “The key cells include keratinocytes, which are known as the surface skin cells. Instead of focusing on barrier repair, they send distress messages, so aren’t focused on barrier repair during this time. Then there are fibroblasts (the ‘support builders’ that make collagen and elastin), which shift to defending when inflammation is present, meaning they make less collagen during this time. Blood vessel cells also allow more immune activity, keeping the area on alert, which can cause problems with barrier function and pigmentation over time.”
Dr Mahto frames it as a constant state of microscopic wear and tear. “Think of acute inflammation (like a cut healing) as a helpful emergency response. The problem arises when this becomes chronic—a low-level, constant hum of irritation that never switches off. When the skin is in this state, it behaves like it is under constant attack.
“To allow immune cells to move around and fight these perceived threats, the skin releases specific enzymes that break down tissue. Unfortunately, these enzymes don’t distinguish between ‘bad’ tissue and your healthy collagen and elastin. Over time, they simply eat away at your skin’s structural support, leading to sagging and wrinkles. It also triggers your pigment cells (which are highly sensitive to stress) to overproduce melanin as a form of self-defence, resulting in uneven tone and sun spots.”
How modern life is inflaming our skin
While ageing itself is inevitable, many of today’s environmental and lifestyle factors are quietly accelerating inflammatory damage. “The biggest contributors to skin inflammation are: UV radiation, which is by far the most damaging,” says Dr Jamil. “It can cause direct DNA damage and can trigger inflammatory responses even without visible sunburn, so it’s important to always wear a broad-spectrum SPF. Pollution also induces oxidative stress and activates aryl hydrocarbon receptor (AhR), which can cause skin inflammation.”
But it doesn’t stop there. “Sleep and stress are daily disruptors to our skin health, as at high levels, or chronic levels, they can impair our barrier repair and alter immune signalling to the skin, which can enhance inflammaging.
Dr Mahto is clear on the biggest offenders: “UV Radiation remains the number one driver. It creates immediate oxidative stress. Pollution is the other big one, especially for those who live in cities.”
Can you have inflamed skin if you’re otherwise healthy?
Inflammation in the skin doesn’t always mirror what’s happening inside the body. “Skin inflammation is not always systemic,’ explains Dr Jamil. “Someone can be healthy, fit and have normal inflammatory blood markers on the outside, but still have low-grade inflammation. This is due to the skin having its own immune and neuroendocrine system, as well as local triggers such as barrier damage, topical irritants and UV damage, which can cause inflammation independently.”
Dr Mahto puts it into perspective: “You can be a marathon runner with a perfect diet, but if you run without sunscreen, your facial skin is undergoing intense inflammatory damage that your internal organs are not. You can have ‘inflamed skin’ on a healthy body simply due to external aggressors like UV and skincare misuse.”
Can skincare slow down inflammaging?
Topical skincare can play a meaningful role—but according to the experts, it has its limits. “Generally, topical skincare works best when inflammation is quite low-grade or mild to moderate, used preventatively and consistently, and your barrier function is not already damaged,” explains Dr Jamil. “Use a broad-spectrum sunscreen and skincare ingredients that help with inflammation include niacinamide, vitamin C, retinoids (slowly), azelaic acid, and ceramides.”
Dr Mahto agrees that ingredient choice is crucial. “Topical skincare is very effective if chosen correctly. Antioxidants (vitamin C, ferulic acid, resveratrol): These are your primary fire extinguishers. They neutralise the free radicals that trigger the inflammatory cascade. While retinoids can be irritating initially for some, in the long-term they thicken the skin and regulate cell function, making the skin more resilient to stress. Azelaic acid is excellent for reducing inflammatory signalling in pigment cells and blood vessels.”
What about injectables and in-clinic treatments?
In-clinic treatments can also influence inflammation in the skin—for better or worse. “Botox indirectly reduces inflammatory signaling due to less muscle contraction which can lower cytokine release,” says Dr Jamil. “Dermal fillers can help with short-term inflammation with well-placed fillers as they can improve fibroblast function. However, be careful as poor technique or overfilling can increase inflammation and make it worse.
Dr Mahto highlights one treatment as particularly useful: “Polynucleotides are explicitly anti-inflammatory. They work by down-regulating inflammatory signals and up-regulating repair. This is why I love them for ‘inflammaged’ skin (like rosacea or sun damage)—they treat the biology, not just the symptom. No other injectables affect inflammation, despite what some marketing claims may make.”