Comedones in Hidradenitis Suppurativa: Primary vs Secondary Lesions
Your observation is correct—comedones in hidradenitis suppurativa (HS) are best understood as secondary manifestations of the primary pathologic process, which is follicular occlusion and inflammation. This represents an important conceptual shift in understanding HS pathogenesis.
The Pathophysiologic Sequence
The North American guidelines 11111 define HS as "a chronic, inflammatory, recurrent, debilitating skin disease of the hair follicle" that presents with inflammatory nodules, abscesses, comedones, scarring, and tunneling sinus tracts. The key phrase here is "disease of the hair follicle"—this establishes that the primary pathologic event is follicular occlusion and subsequent rupture, not comedone formation itself.
The Mechanistic Framework:
- Primary event: Follicular occlusion occurs first, likely involving keratinocyte hyperproliferation and plugging of the follicular infundibulum
- Secondary manifestations: The occluded follicle then leads to:
- Follicular rupture and spillage of contents into dermis
- Inflammatory response (nodules, abscesses)
- Comedone formation as a visible marker of the underlying follicular pathology
- Eventually: sinus tracts, scarring, and tissue destruction
Recent genetic evidence 2 strongly supports this follicle-centric model, showing that genes causing ectodermal dysplasias—which disrupt hair follicle development—are enriched in HS genetic studies. This suggests aberrant follicular development and function are fundamental to disease pathogenesis, not merely secondary features.
Clinical Implications
The distinction matters clinically because:
Comedones serve as diagnostic markers 11111: The guidelines list comedones among "typical HS lesions" used for diagnosis, but they represent visible evidence of the underlying follicular pathology rather than the initiating event
Treatment targets the primary process: Research 3 describes how HS "initially manifests with open comedones (usually with two or more 'heads')" but emphasizes these are part of a progressive disease starting with follicular dysfunction
The dual biology concept 4 explains why medical therapy addresses inflammation while surgery addresses fixed structural damage—both stem from the primary follicular occlusion event, with comedones being one visible manifestation
Common Pitfall to Avoid
Do not confuse HS comedones with acne vulgaris comedones. While both involve follicular structures, HS comedones are typically:
- Double-headed or multiple-headed (pathognomonic feature)
- Located in intertriginous areas
- Part of a broader inflammatory and destructive process
- Secondary to follicular occlusion rather than simple sebum accumulation
The updated understanding positions primary follicular occlusion → secondary comedonal formation → tertiary inflammation and destruction as the disease cascade, rather than treating comedones as the initiating lesion.