Persistent colonization and inflammatory signaling
Bacterial biofilm is a structured microbial community encased in a protective matrix that enables persistent colonization and toxin production. Within the eyelid, biofilm can sustain chronic inflammation by shielding bacteria from host defenses and reducing susceptibility to topical therapies.
- Protected microbial persistence
- Ongoing inflammatory stimulus
- Reduced response to surface-level approaches
The model emphasizes upstream inflammatory source control rather than downstream symptom suppression alone.
Inflammation beneath the lid margin
Deep Subdermal Blepharitis represents a chronic inflammatory disease state affecting eyelid tissues beneath the lid margin. Unlike superficial blepharitis, DSB involves intraglandular inflammation that cannot be adequately addressed through surface-level treatment alone.
DSB is framed as a deeper inflammatory process that can drive persistent gland dysfunction when left unaddressed.
Surface findings can coexist with deeper inflammation, requiring a model that accounts for intraglandular disease dynamics.
When the inflammatory source persists, obstruction and tissue injury can progress despite symptomatic therapies.
A visible indicator of deep inflammation
The Rynerson Red Line is a clinically observable marker of deep subdermal inflammation. Its presence and intensity are used to correlate with disease severity and provide a practical tool for diagnosis and monitoring of treatment response.
A visible feature that can be monitored over time within standard clinical workflows.
Used to help contextualize the depth and persistence of inflammatory activity.
Supports longitudinal monitoring when paired with symptom and gland function assessment.
From chronic inflammation to gland dropout
Chronic inflammation alters meibum composition, leading to ductal obstruction, increased intraglandular pressure, and progressive acinar cell damage. Over time, this process can result in gland dropout and persistent tear film instability.
Ongoing inflammatory signaling contributes to sustained tissue stress within and around glands.
Composition changes and ductal compromise increase resistance to flow and expression.
Increased intraglandular pressure contributes to structural stress and progressive acinar damage.
Gland loss is associated with chronic tear film instability and persistent symptoms.
Source control, sequencing, and durability
Effective long-term disease control requires addressing the inflammatory source rather than downstream symptoms alone. This scientific framework supports protocolized intervention strategies designed to restore gland function and limit disease progression.
Prioritize reduction of the drivers of chronic inflammation.
Sequencing is used to improve consistency and repeatability.
Monitoring supports interval planning and refinement over time.
This content describes a disease model and clinical rationale. It does not constitute medical advice or universal treatment claims.