Biomimetic medical adhesives

Every industrial adhesive is designed for a dry, rigid, chemically inert surface. Tissue is none of these. It is covered by a bound hydration layer, it is mechanically soft, it moves with every heartbeat and breath, and it renews itself — the surface a surgeon glues today is partly gone in a week. A medical adhesive therefore does not fail for lack of chemical bonding energy; it fails because the bonds never reach the substrate, or because what they hold is peeling away from underneath.

Displacing the water

The first problem is interfacial. Water is not a contaminant to be wiped off; it is hydrogen-bonded to the tissue surface and thermodynamically reluctant to leave. Any adhesive that relies on hydrogen bonding alone competes with water on water’s own terms and loses.

Marine organisms solved this, and biomimetic chemistry has largely converged on their solution. Mussel foot proteins contain L-DOPA, produced by post-translational hydroxylation of tyrosine. The resulting catechol — two adjacent hydroxyls on an aromatic ring — is unusually good at getting to a wet surface: it forms bidentate hydrogen bonds, coordinates strongly to metal oxides and to iron, and can displace the interfacial water rather than merely sit on it. This is why catechol-functionalised polymers recur across otherwise unrelated products.

The sandcastle worm contributes the delivery half. Its cement is a complex coacervate — oppositely charged polyphosphoserine and polybasic proteins phase-separating into a dense fluid with very low interfacial tension against water. A coacervate does not disperse when injected into a wet field; it spreads and wets the surface before it sets. That is a formulation principle, not a chemistry one, and it is why some sealants are injected as fluids that would be useless as a film.

The trade-off that sets the ceiling

Catechol adhesion carries a built-in conflict. Oxidised to a quinone, catechol becomes reactive and crosslinks with amines and thiols, giving the bulk material cohesive strength. But the same oxidation consumes the reduced catechol that was doing the surface binding. Adhesion and cohesion draw on one chemical pool, and a formulation strong internally tends to be weakly attached. Mussels manage this by segregating chemistry in space and time — a cysteine-rich protein maintains the reduced state at the interface — which synthetic single-pot systems find hard to reproduce.

Two further constraints are mechanical rather than chemical. A stiff adhesive on soft tissue concentrates stress at the edges of the bond, so a modulus-mismatched sealant delaminates under cyclic load even when its shear strength on a test coupon looks excellent. And an adhesive must degrade on the timescale that healing takes: too slow and it becomes a foreign body, too fast and it releases the repair before the tissue holds.

These are why bench numbers translate badly. Burst-pressure testing under ASTM F2392 or wound-closure strength under ASTM F2458 is measured on a substrate that does not bleed, move or remodel. Under EU MDR 2017/745 the demonstration that matters is clinical performance in a specific indication — and indications differ far more than the chemistry does.