Foreign Body Response (FBR) Mechanisms in CGMs

Foreign Body Response (FBR) in Continuous Glucose Monitors (CGMs)

Introduction

The foreign body response (FBR) is the body's attempt to wall off anything implanted under the skin, and it is one of the main reasons a CGM sensor drifts and wears out. A review of implantable enzyme sensors names it a prominent cause of implanted sensor failure [5]. It begins with the injury of insertion. It then lasts as long as the device stays in the body [1]. Our CGM article on biofouling and foreign body response mitigation covers the fixes in more depth.

Phases of FBR

Pathologists describe a long chain of reactions after implantation, from injury and inflammation through granulation tissue to a fibrous capsule [1]. For a glucose sensor, three stages matter most:

• Protein Adsorption: Proteins from blood and tissue fluid coat the sensor surface first, a process called biofouling [1]. In lab tests, this protein layer acted as a diffusion barrier that slowed glucose on its way to the sensor [4].
• Acute Inflammation: Neutrophils, a type of white blood cell, are the hallmark of this stage [1]. When researchers exposed glucose sensors to activated granulocytes (the white-cell family that includes neutrophils), the cells released substances that used up the hydrogen peroxide the sensor measures, and the signal dropped [4].
• Fibrosis: Macrophages and foreign body giant cells (macrophages fused together) settle on the surface, and the tissue around them matures into a fibrous capsule that can interfere with how an implanted device works [1].

Impact on Glucose Sensors

Most CGMs worn on the skin measure glucose with the enzyme Glucose Oxidase (GOx), and that reaction needs oxygen [2]. So anything near the filament that shifts local oxygen or glucose can shift the reading. The authors of a 2018 study noted that cells and drugs near a sensor have been shown to do exactly that, while adding that the exact cause of early CGM noise is still unclear [2]. In their mouse and monkey experiments, uncoated sensors were already noisy within the first day after implantation [2].

Later, the capsule becomes the bigger problem. A modeling study found capsule thickness was the strongest driver of physiological lag, the delay between a change in blood glucose and the same change at the sensor [3]. Blood vessel density and capsule porosity mattered most for how much glucose reached the sensor at all [3]. Not every CGM uses GOx, though: the implanted Eversense 365 reads glucose by fluorescence [6].

Combating FBR

Here's what we found when we looked for evidence that manufacturers use zwitterionic coatings: the clearest source is a research study, not a product label. In 2018, a team coated commercial Medtronic CGM sensors with a zwitterionic polymer, a class of material known for resisting protein adsorption [2]. The coating cut signal noise and inflammation in mice and non-human primates, and the coated sensors tracked glucose without recalibration [2].

Drug elution, by contrast, is on the market. The Eversense 365 sensor carries a silicone collar that releases 1.75 mg of dexamethasone acetate, an anti-inflammatory steroid, to minimize the local foreign body reaction, and FDA cleared it in September 2024 for up to 1 year of wear [6].

Wear time has grown a lot. Dexcom's STS sensor, approved in 2006, was labeled for up to 72 hours [7]. As of October 2026, the MiniMed Simplera CGM lasts up to 6 days [9]. The Dexcom G7 lasts 10 days and the Dexcom G7 15 Day sensor 15 days [8], while the implanted Eversense 365 lasts up to a year [6]. Controlling the FBR is only part of that progress; a 2012 review also lists enzyme stability, calibration and power requirements among the hurdles for long-term sensors [5].