Proteoglycan Follicular Atrophy

 

Proteoglycan Follicular Atrophy is today a clinically established pathology and is a condition where a wasting away of selective proteoglycans from the dermal papilla, the inner and outer root sheath, occurs, coupled with an ever-decreasing ability of the body to reproduce these in a normal, healthy manner.

 

Proteoglycan Follicular Atrophy develops gradually and progresses through five distinct stages.

1Dysregulated Follicle

Unlike the Anagen (growth) phase in a healthy hair follicle, where proteoglycan levels are sufficient to support a full growth phase, depletion of proteoglycans in a hair follicle affected by Proteoglycan Follicular Atrophy shortens the duration of the Anagen phase. 

 

This disruption of the normal hair growth cycle prevents the follicle from producing a hair shaft to its full length and thickness. The depletion of proteoglycans causes premature transition out of the Anagen phase, leading to progressive follicular miniaturisation and weakened hair growth.

2Early Stage Hypo-Glycania

As proteoglycan levels continue to deplete within the follicles, an increasing number of hairs prematurely transition into the Telogen (resting) phase. This prolongs the normal resting phase and leads to increased hair shedding.

 

A prolonged resting phase means that fewer hair follicles re-enter the Anagen (growth) phase, resulting in weaker regrowth or complete absence of hair strand production. These follicles are often referred to as dormant or “sleeping” hair follicles.

3Late Stage Hypo-Glycania

As proteoglycan levels fall below the critical threshold, the follicle experiences cellular starvation.

 

Deprived of the necessary proteoglycan signalling, the follicle enters a late stage of Follicular Hypo-Glycania. In this state, the follicle is unable to function or regenerate properly.

4Prolonged Hypo-Glycania

When the follicle remains in a prolonged state of Follicular Hypo-Glycania, the resulting damage becomes irreversible. The last follicular proteoglycans that drive and regulate the hair cycle progressively degrade, leaving the follicle unable to support active hair growth.

 

Prolonged Follicular Hypo-Glycania leads to irreversible follicular damage, ultimately resulting in Proteoglycan Follicular Atrophy.

5Atrophied Follicle

When a hair follicle enters the stage of atrophy, it means the follicle has ceased functioning and can no longer produce a hair strand. At this point, the follicle is considered dead.

 

Hair transplantation becomes the only viable treatment option once a follicle has reached this stage. It is therefore vital that Proteoglycan Replacement Therapy is introduced in the earlier stages of the hair growth cycle.

Proteoglycan Follicular Atrophy unbalances the normal regulated Hair Growth Cycle by shortening the Anagen phase, initiating an early Catagen phase, and prolonging the Telogen phase. This imbalance contributes to the disruption of the hair growth signal.

The Impact of PFA on the Hair Growth Signal

1Cycle 1

Proteoglycan Follicular Atrophy occurs when key proteoglycans in the dermal papilla gradually decline, weakening Wnt signalling while Dkk1 activity remains steady. As shown in the diagram, this disruption of the hair growth cycle progresses across three successive cycles. 

 

In the first cycle, reduced proteoglycan levels shorten the Anagen (growth) phase, which promotes an earlier transition into Catagen – the brief transitional phase that leads into the Telogen (resting) phase. Although Anagen is shortened in this cycle, it remains long enough to produce a visible hair. 

2Cycle 2

As the cycle restarts and proteoglycan levels decline further, the Anagen phase becomes even shorter, and Catagen is entered more rapidly, meaning that the transition into Telogen occurs sooner and is prolonged, resulting in the formation of a thin, vellus hair.

3Cycle 3

By the third cycle, Anagen has become too short to sustain any growth, with the follicle rapidly transitioning through Catagen into an extended Telogen phase. In this cycle, no visible hair is produced. 

 

This progressive shortening of Anagen, earlier entry into Catagen, and prolongation of Telogen across repeated cycles reflects a disrupted hair growth cycle driven by Proteoglycan Follicular Atrophy.

The Impact of Proteoglycan Follicular Atrophy on the Hair Growth Signal

Proteoglycan Follicular Atrophy occurs when key proteoglycans in the dermal papilla gradually decline, weakening Wnt signalling while Dkk1 activity remains steady. As shown in the diagram, this disruption of the hair growth cycle progresses across three successive cycles. 

 

In the first cycle, reduced proteoglycan levels shorten the Anagen (growth) phase, which promotes an earlier transition into Catagen – the brief transitional phase that leads into the Telogen (resting) phase. Although Anagen is shortened in this cycle, it remains long enough to produce a visible hair. 

 

As the cycle restarts and proteoglycan levels decline further, the Anagen phase becomes even shorter, and Catagen is entered more rapidly, meaning that the transition into Telogen occurs sooner and is prolonged, resulting in the formation of a thin, vellus hair.

 

By the third cycle, Anagen has become too short to sustain any growth, with the follicle rapidly transitioning through Catagen into an extended Telogen phase. In this cycle, no visible hair is produced. 

 

This progressive shortening of Anagen, earlier entry into Catagen, and prolongation of Telogen across repeated cycles reflects a disrupted hair growth cycle driven by Proteoglycan Follicular Atrophy.

Nourkrin® with Marilex® is a bioactive proteoglycan formula used as a Proteoglycan Replacement Therapy and is specifically designed to normalise the Hair Growth Cycle and promote normal, healthy hair growth.

 

 

Read more about Proteoglycan Replacement Therapy