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An energetic neutron can collide with a lattice atom and create a primary knock-on atom. That recoil transfers energy to other atoms in a displacement cascade. Some atoms leave their normal lattice sites, creating Frenkel pairs: a vacancy and an extra atom at an interstitial position.

Many nearby defects recombine during the cascade and its thermal relaxation. The surviving point defects are therefore fewer than a simple count of all displacement events. Some defects are already clustered within the cascade; others migrate and aggregate later.

A collection of vacancies can collapse into a platelet bounded by a vacancy-type dislocation loop. An aggregation of self-interstitial atoms can create an extra atomic platelet bounded by an interstitial-type dislocation loop. The boundary is a line defect because a circuit around it has a nonzero Burgers vector. The allowed Burgers vectors and habit planes depend on the material's crystal structure and fault energies.

Loops can grow by absorbing mobile point defects, shrink by emitting or absorbing the opposite defect type, and interact with existing dislocations. Some remain faulted, while suitable loops can unfault or become part of a larger dislocation network. Repeated cascades and subsequent defect transport therefore create a population of extended defects even in material with a low initial dislocation density.

This describes the main displacement-damage mechanism. Ionizing energy deposited in a material does not automatically create the same defect population as a neutron recoil cascade; recoil spectrum, displacement thresholds and material response matter.

The resulting dislocation density reflects competing production, growth and recovery rates. The irradiation spectrum and displacement dose rate set the supply of recoil cascades and surviving point defects. Cascade structure controls the fraction born as isolated defects or clusters; equal nominal displacements per atom can therefore give different defect populations.

Temperature sets vacancy and interstitial mobilities and the rates of thermal emission and recovery. A simple radiation damage rate theory model illustrates the competition using number densities $c_i,c_v$:Here $G$ is the surviving mobile-pair production rate per volume, $K_{\mathrm{rec}}$ is the recombination coefficient, $D_i,D_v$ are diffusion coefficients, and $k_i^2,k_v^2$ are sink strengths. The model omits explicit cluster-size populations and thermal-equilibrium emission; those must be added for a quantitative description of a particular exposure.

The initial dislocation density, grain size, free surfaces, precipitates and existing cavities all change sink strengths. Dislocations can have an interstitial bias, so their capture rates for the two defect types differ. Solutes and transmutation gases alter defect binding and mobility. Crystal structure, elastic anisotropy and applied stress affect which loop orientations survive and grow.

For a number density $N_{\ell }$ of circular loops of radius $R$, their contribution to line length per volume isThus loop nucleation and loop growth both increase dislocation density, while shrinkage, annihilation and absorption at other sinks can decrease it. A change in loop count alone does not determine the change in total line density.

Schematically, ${\dot{\rho }}_d$ is a production-and-growth contribution minus recovery and annihilation. An initial rise followed by approximate saturation is possible when these balance, but the saturation value and approach rate depend on the evolving microstructure. There is no universal dislocation density fixed by dose alone.

Annihilation of a vacancy and an interstitial, or related relaxation of irradiation defects. The surviving damage after a cascade can be much smaller than its initial number of atomic displacements.

An extra atom of the host material accommodated outside the ordinary lattice-site inventory. It can migrate, recombine with a vacancy, or join a cluster.