INTRODUCTION
Dandruff is a common skin condition affecting up to half of the world’s population. Symptoms include pruritus, inflammation, and flaking. It is thought to be in part due to microbe dysbiosis.
This paper aims to discuss the relationship between dandruff and Cutibacterium acnes (C. acnes). It will also explore the potential role of C. acnes’s biofilm in the formation of the biological glue that sticks dandruff flakes together.
Overview of Dandruff
Dandruff is a common scalp disorder affecting between 17 to 50% of the population.1 Dandruff describes the abnormal flaking of the scalp due to mild inflammation. In this abnormal flaking, the stratum corneum demonstrates disrupted corneocyte cohesion and cell hyperproliferation.1
Dandruff typically begins around puberty and is associated with flaking, pruritus, and inflammation. The skin of the scalp is highly innervated and vascularized. Within the scalp skin, most epithelial cells are hair follicle keratinocytes.2 These cells exhibit secretory activity that extends into dermal adipose tissue. They also produce β-endorphin and endovanilloids, which are pruritogenic neuromediators and help to create the pruritic sensation associated with dandruff.2
Dandruff is related to seborrheic dermatitis, which has similar symptoms but unlike dandruff, seborrheic dermatitis is not restricted to the scalp. Dandruff is also similar to psoriasis in that it exhibits parakeratosis and the dandruff flakes themselves exhibit neutrophil-chemotactic anaphylatoxins.2
Explanations for dandruff include over-colonization with yeast, imbalance of bacterial microbiome, disrupted epidermal barrier function, increased sebum-derived fatty acid metabolites, peroxidation of squalene, and perivascular leukocyte infiltration. This can lead to increased proliferation of the basal layer epidermal keratinocytes.2 This increases corneocyte production and shedding, which produces the clinical manifestation recognized as dandruff.2
Overview of Cutibacterium Acnes
C. acnes is a lipophilic, gram-positive, facultative anaerobe.3 C. acnes makes up less than 2% of skin bacteria and is mainly found deep within the sebaceous glands.4 It preferentially lives on the skin of the face, back, and chest due to the high concentration of sebum in these areas.4
C. acnes plays a role in maintaining homeostasis. C. acnes is able to break down sebum-consistent triglycerides into smaller fatty acids, including propionic acid, which helps to keep the skin at an acidic pH. By helping to maintain an acidic pH, it helps protect from other bacteria, including Staphylococcus aureus.4 Cutibacterium secretes bacteriocin, which can also inhibit the growth of Staphylococcus. At the same time, Staphylococcus can ferment glycerol, which can inhibit the growth of Cutibacterium.5
This paper aims to discuss the relationship between dandruff and Cutibacterium acnes (C. acnes). It will also explore the potential role of C. acnes’s biofilm in the formation of the biological glue that sticks dandruff flakes together.
Overview of Dandruff
Dandruff is a common scalp disorder affecting between 17 to 50% of the population.1 Dandruff describes the abnormal flaking of the scalp due to mild inflammation. In this abnormal flaking, the stratum corneum demonstrates disrupted corneocyte cohesion and cell hyperproliferation.1
Dandruff typically begins around puberty and is associated with flaking, pruritus, and inflammation. The skin of the scalp is highly innervated and vascularized. Within the scalp skin, most epithelial cells are hair follicle keratinocytes.2 These cells exhibit secretory activity that extends into dermal adipose tissue. They also produce β-endorphin and endovanilloids, which are pruritogenic neuromediators and help to create the pruritic sensation associated with dandruff.2
Dandruff is related to seborrheic dermatitis, which has similar symptoms but unlike dandruff, seborrheic dermatitis is not restricted to the scalp. Dandruff is also similar to psoriasis in that it exhibits parakeratosis and the dandruff flakes themselves exhibit neutrophil-chemotactic anaphylatoxins.2
Explanations for dandruff include over-colonization with yeast, imbalance of bacterial microbiome, disrupted epidermal barrier function, increased sebum-derived fatty acid metabolites, peroxidation of squalene, and perivascular leukocyte infiltration. This can lead to increased proliferation of the basal layer epidermal keratinocytes.2 This increases corneocyte production and shedding, which produces the clinical manifestation recognized as dandruff.2
Overview of Cutibacterium Acnes
C. acnes is a lipophilic, gram-positive, facultative anaerobe.3 C. acnes makes up less than 2% of skin bacteria and is mainly found deep within the sebaceous glands.4 It preferentially lives on the skin of the face, back, and chest due to the high concentration of sebum in these areas.4
C. acnes plays a role in maintaining homeostasis. C. acnes is able to break down sebum-consistent triglycerides into smaller fatty acids, including propionic acid, which helps to keep the skin at an acidic pH. By helping to maintain an acidic pH, it helps protect from other bacteria, including Staphylococcus aureus.4 Cutibacterium secretes bacteriocin, which can also inhibit the growth of Staphylococcus. At the same time, Staphylococcus can ferment glycerol, which can inhibit the growth of Cutibacterium.5
