There are numerous skin anomalies that are observed with clients throughout the course of a professional’s practice. Identifying them, their underlying causes and possible remedies requires an understanding of the science of the skin, organs, and their disorders and diseases. Moreover, knowledge of performing a thorough assessment and possible reasons for the occurrence of various nodules, depressions, lesions, and pilosebaceous (hair follicle) abnormalities requires further study.
Sebaceous hyperplasia are small, yellowish growths that develop on the skin, normally on the face. It is one of many clinical forms of hyperplasia.1

EXPLORING HYPERPLASIA

First, it is important to understand hyperplasia, generally. The term hyperplasia (Greek, “hyper” meaning “over” and “plasis” meaning “formation”) is defined as the enlargement of an organ or tissue caused by an increase in the reproduction rate of cells. It is also referred to as hypergenesis, an increase in the amount of organic tissue resulting from cell proliferation. Hyperplasia occurs after a response to a stimulus whereby there is an increase in the number of normal cells due to increased demand.2 Hyperplasia may be physiological or pathological.

Physiological

Physiological hyperplasia is the normal response to a specific subject to regulatory control mechanisms such as hormones. Cells remain the same size, but increase in number. An example of stimuli would be a hormonal increase or growth factor, such as the female breast during puberty or in pregnancy for the proliferation of milk-secreting glandular cells in the breast. Hyperplasia occurs in the endometrium during the proliferation phase of a menstrual cycle. Another example is the proliferation of the basal layer in the epidermis to counteract skin loss or chronic inflammatory response, or to compensate damage or disease in other parts of the body.3

Pathological

Pathological hyperplasia occurs if there is an excess of hormone or growth factor stimuli during the presence of disease. such as in the prostate gland during aging. Hyperplasia in the endometrium is a result of a hormone producing an ovarian tumor. Hyperplasia of the breast manifests as hyperplastic lesions in the breast that may lead to a more abnormal pattern of growth, increasing cancer risk. Hyperplasia in adrenal glands manifests as pituitary tumors. Hyperplasia in parenchymal organs in acromegaly is abnormal growth of hands, feet, and face caused by overproduction of growth hormone by the pituitary gland.

DYSPLASIA – DYSFUNCTIONAL CELL GROWTH

Abnormal stimuli can lead to dysplasia involving the dysfunctional cell growth during morphological changes. There are four ways cells can become dysplastic: with hypertrophy, cells can grow large in size; hyperplasia can stem from an increase in cell number; in atrophy, cells can decrease or shrink in number; and with metaplasia, cells can change type.4

These changes occur due to some of the normal stimuli to cells and can be non-carcinogenic, such as chronic irritation from smoke. In dysplasia, the cells can look abnormal under a microscope, however may not be cancerous. Hyperplasia and dysplasia may or may not become cancer.1

The stimuli could also be carcinogenic, which may cause genetic damage to the cells. Dysplasia is often part of the pre-malignant process. As an example, stratified squamous cells are bound to the basement membrane. With an abnormal stimulus, such as a genetic abnormality, cells lose general regulation of growth, proliferation, and ability to differentiate. They begin with a low-grade dysplasia and are not too different from the original cells. Without removal of the stimulus, however, the dysplasia gets worse, moving from medium to high grade dysplasia. The cells become very different from their original state and neoplastic cells may develop where an abnormal growth of tissue forms called a tumor. High-grade dysplasia can become cancerous.

SEBACEOUS HYPERPLASIA

Sebaceous hyperplasia is a benign and non-contagious condition that occurs when sebaceous glands become enlarged with trapped sebum. It may be more common during middle-age and among the elderly. Individuals who have had more sun exposure are more likely to get it. There may also be a genetic component to this condition. Sebaceous hyperplasia is more prevalent in immunosuppressed patients and those on immunosuppressant medication, such as cyclosporine.5

Lesions can be single or multiple – as well as slightly yellowish and soft – with small papules on the face around the cheeks, nose, and forehead. They can also appear as a basal cell, thus may require medical diagnosis to verify. Closer examination shows sebaceous hyperplasia as being depressed or pitted at the center of the lesion. They are sometimes confused with comedonal acne. Moreover, they can become irritated if attempts are made to extract them.

THE HAIR FOLLICLE

The pilo-sebaceous unit (hair follicle) contains sebaceous glands that excrete sebum through a duct system into the follicle. Sebum travels up the hair shaft onto the surface of the skin where it becomes part of the mix of microflora of the acid mantle. Cells that form the sebaceous gland are called sebocytes and begin their life cycle in the highly mitotic basal cell layer. During the maturation and differentiation of sebocytes they increase amounts of lipid that migrate toward the central excretory duct. At this point, they release their lipid contents into the follicle.6 

Sebaceous glands are very androgen sensitive. Their activity and size may vary dependent upon age and circulating hormone levels.7 Sebaceous and sweat glands account for most of the androgen metabolism in the skin.

Sebocytes contain androgen-metabolizing enzymes – 5-alpha-reductase type 1, 3 beta-hydroxysteroid dehydrogenase, and 17-beta hydroxysteroid dehydrogenase type II. The enzymes metabolize weaker circulating androgens into the more potent androgens that bind to receptors within the sebocytes, causing an increase in the size and metabolic rate of the sebaceous gland. The activity of 5-alpha-reductase is higher in the scalp and facial skin. Testosterone and dihydrotestosterone stimulate more sebaceous activity.

Androgens stimulate the sebaceous glands, especially during puberty. During the aging process, androgen hormones decrease.8 The sebaceous gland activity decreases, as well as the natural cell turnover. There may be a backup of sebocytes within the gland resulting in enlargement of the gland.

TREATMENT AND CARE

It is very difficult to eradicate sebaceous hyperplasia completely, since it is a systemic condition. Topical retinoids and azelaic acid have been employed to assist in preventing the sebaceous hyperplasia from forming, since they assist in the skin’s natural desquamation rate. Medical intervention using laser or excision may make some improvement. However, there is risk of scarring or skin discoloration. It is more about keeping these conditions under control through maintaining optimum health in the skin.

A more pro-active approach for improving the appearance of the skin begins with understanding the biological changes and alterations that occur during the aging process, especially post-menopause. There is a mitigation of cell signaling and metabolic rate. It is imperative to maintain a healthy lifestyle through good nutrition; consuming anti-inflammatory foods, antioxidants, and essential fatty acids; adequate intake of water; and rest. Reduce stress levels through massage therapy, walking, and mindful practices, such as yoga and meditation. Perform treatments that support the health of the skin, maintaining the integrity of the barrier function. Avoid the use of aggressive treatments that compromise or wound the skin. It is more important to be mindful of supporting the underlying structures of the skin in the dermis and epidermis through treatment that encourages the skin’s natural repair mechanisms. The use of enzymes, nourishing serums, and rejuvenating treatments utilizing microcurrent or LED have proven effects for rebuilding collagen and reducing inflammation with marked improvement of the appearance of the skin.

Home care should be biomimetic to the skin utilizing vitamin A, C, and E, as well as peptides, phytoextracts, and natural lipids. Ceramides, fatty acids, and shea butter (contains phosphatidylcholine) are examples of ingredients that support the health of the skin.

References
1 National Cancer Institute Dictionary of Cancer Terms, s.v. “Hyperplasia,”
https://www.cancer.gov/publications/dictionaries/cancer-terms/def/hyperplasia.
2 5MinuteSchool. “Hyerplasia - Physiological vs Pathological | Explained in 2 Minutes!”.
YouTube video, 2:09. Posted [Oct. 2016]. https://www.youtube.com/watch?v=-jzJqpf1xnE.
3 Wikipedia, s.v. “Hyperplasia,” last modified May 8, 2018,
https://en.wikipedia.org/wiki/Hyperplasia.
4 Learn Oncology. “Dysplasia: The Progression of Cancer”. YouTube video, 4:19. Posted [July
2015]. https://www.youtube.com/watch?v=Gh_1PfLKqg4.
5 Oakley, Amanda, Vanessa Ngan, and Clare Morrison. “Sebaceous hyperplasia.”  DermNet NZ.
https://www.dermnetnz.org/topics/sebaceous-hyperplasia.
6 Robles, David T. “Sebaceous Hyperplasia.” Medscape.
https://emedicine.medscape.com/article/1059368overview#a5.   
7 Ibid
8 Palmer, Angela. “Sebaceous Hyperplasia Causes, Symptoms, and Treatments.” Verywell
Health. https://www.verywellhealth.com/sebaceous-hyperplasia-causes-symptoms-and-
treatments-4144250.

Alexandra J. Zani is an international educator, researcher, and author with a background in cell biology and medicine. Her passion for education resulted in receiving numerous advanced certifications, both in the United States and abroad. Zani earned an instructor license for aesthetics/cosmetology, is NCEA certified, certified in Oncology Esthetics®, and the Pastiche Method® of Skin Analysis. She is a member of the International Association for Applied Corneotherapy (IAC). Zani presents education for advanced aesthetic technology, including microcurrents, LED, and non-ablative laser. She is a specialist in the anti-aging sciences, including the effects of nutrition, lifestyle, and the mind/body connection.