Michelle Tarbox, MD

Follicular occlusion, anaerobic biofilm, and innate immune activation combine to drive tissue destruction. The panel explains why tunnels sustain inflammation and mark the transition from acute disease to irreversible scarring.

HS Pathophysiology: Follicular Occlusion, Biofilm, and Innate Inflammation

"HS Pathophysiology: Follicular Occlusion, Biofilm, and Innate Inflammation" takes up the question of what drives tissue destruction in HS and why tunnels behave differently from nodules.

The panel is asked to describe the pathophysiology of HS and what drives the changes seen in patients. The panel identifies follicular occlusion and hyperproliferation of the epithelium as the primary events. Under the microscope, the tunnels resemble a very angry, inflamed psoriasis, although they do not behave identically because the tunnel is a sequestered anaerobic environment. Secretions, dead keratinocytes, and skin oils serve as a food source for anaerobic bacteria, which leads to biofilm formation. The resulting inflammation is driven largely by the innate immune system, which is fast and vicious by design. When it misfunctions in this way, cytokines such as TNF-alpha, IL-1 beta, IL-17, and IL-36 rise, creating a perfect storm that destroys tissue. The panel also stresses that the disease is multifactorial. Neutrophils and B cell inflammation within the follicular epithelium of the tunnels are part of the picture, and the panel suggests the field is only scratching the surface of what is still to come.

The discussion then moves to what makes tunnels different from an isolated nodule. The panel explains that a biofilm will always be present in a tunnel for as long as it remains inflamed, because the hyperproliferative epithelium produces too much food for bacteria to go unnoticed. Biofilms resist both the immune system and antimicrobial agents. The anaerobic environment also explains why enteric pathogens grow out of tunnels, a finding that can surprise clinicians early in their careers. These pathogens are highly immunostimulatory, so inflammation keeps accelerating and damages native tissue. Structural damage then becomes irreversible, marking the shift from an acute inflammatory disease to a chronic, scarring one.

"HS Draining Tunnels: Severity Markers, Scarring, and Unmet Needs,"

 the experts discuss what draining tunnels signal about severity and progression.

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Delayed recognition of HS costs patients time, tissue, and quality of life. The panel examines why episodic flares and atypical presentations are missed and the shame and isolation that follow.

HS Diagnostic Delay: Why It Persists and the Psychosocial Burden

Welcome back to another HCPLive Peer Exchange series. In "HS Diagnostic Delay: Why It Persists and the Psychosocial Burden," moderator Martina Porter, MD is joined by Ali Shahbaz, MD, FAAD, FRCPC and Michelle Tarbox, MD to open the series on hidradenitis suppurativa.

Moderator Dr. Porter opens by noting that HS is often associated with a substantial diagnostic delay, in some studies up to 10 years, and asks why the disease remains under-recognized. The panel points first to its episodic course, with flares alternating with periods of remission. Patients frequently present to emergency or urgent care settings, where each flare is treated as an isolated abscess and the underlying pattern goes unrecognized. The affected areas are also private, and patients may understandably feel uncomfortable discussing them with a new physician, which places much of the responsibility on clinicians to be well educated about the disease.

The panel frames the cost of delay in three parts: lost time and productivity at work, lost functional tissue that is exchanged for tunnels and scarring, and lost ability to participate fully in life. Presentation also varies. Patients seen during an acute flare offer the best chance of a correct diagnosis, while atypical presentations in areas patients have not yet felt comfortable sharing can require several follow-up visits. Earlier-onset patients who do not fit the classic picture are especially likely to go unrecognized.

The discussion then turns to burdens beyond visible lesions. The panel describes shame as an unseen weight that patients carry into the office, with the burden often falling on them to seek a diagnosis. Pain, malodor, and drainage add a second layer of impact. HS can also be isolating, particularly when patients do not realize the lesions are not contagious and withdraw from the people they care about. The panel links this to lost relationships, missed work, and missed life events, along with the constant anxiety of living with the disease.

"HS Pathophysiology: Follicular Occlusion, Biofilm, and Innate Inflammation,"

 turns to the inflammatory and microbial mechanisms that make HS tunnels so destructive.

Michelle Tarbox, MD

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