Edema occludes the mouth of the follicle, which continues to expand, rupturing into the underlying fatty tissue. Keratin and pus escape, and a foreign body reaction results in a microabscess, which is similar to perforating folliculitis. The purulent material subsequently tracks within the presacral subcutaneous tissue, producing acute and chronic pilonidal abscesses, as well as potential laterally displaced and epithelialized tracts. It was once thought that every pilonidal lesion contained a nest of hair. This finding, however, does not diminish its importance in the pathophysiology of pilonidal disease.
Hair has three distinct roles.
The distended hair follicle plays the first role. The hair contributes to local inflammation once the follicle ruptures, and it can even perforate the posterior wall of the follicle, enhancing microabscess formation. The second role is that of hairs from other parts of the body, which also can cause local disease. Free hairs act as secondary invaders, entering the follicle through its open mouth and contributing to the foreign body reaction. Neighboring hair in the skin surrounding pilonidal wounds plays the third role.