Chapter 8: Dermatological Health and Disease

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Human Dermatological System

The dermatological system also referred to as the integumentary system or skin, is the largest organ in the body. It also includes the hair and nails, which are appendages of the skin. Skin and hair provide a protective layer from harmful ultraviolet radiation and sunburn. It even cushions and protects the body from infection. The system regulates body temperature and is the initial defense against bacteria, viruses and other microbes. The human skin color is determined by the interaction of melanin, carotene, hemoglobin and is dependants on geographical and climate factors. The dermatological system stores water, fat, glucose and vitamin D. Human skin is made up of three tissue layers:

  1. Epidermis: is the first layer of skin that does not contain any blood vessels.
  2. Dermis: is the central layer of skin, which provides elasticity and is composed of papillary and reticular layers.
  3. Hypodermis: is the most buried layer of skin, it insulates the body, shields the internal organs and is composed of adipose tissue (storage of excess energy in the form of fat).

Throughout the dermatological system, the endocannabinoid system facilitates both immunological and nervous system responses by the dispersed CB1 and CB2 receptors. Therefore an endocannabinoid deficiency may affect dermatological constituents, leading to skin and underlying tissue diseases and complications.1, 4, 7, 9, 12

Role of CBD in Dermatological Diseases

Chronic and severe dermatological conditions such as eczema, psoriasis, and dermatitis cause symptoms that include rash, pruritus (severe itching), a higher risk of infection and possible psychological stress. Signs of dermatitis become more pronounced with the immunological response. CB1 and CB2 receptors can reduce these symptoms in a clinical endocannabinoid deficiency if activated with the administration of cannabidiol. Studies promote the anti-inflammatory and analgesic properties of CBD in reducing symptoms. Moreover, the ability of CBD to inhibit keratinocyte proliferation makes it a potential treatment for dermatological diseases such as psoriasis. Psychological stress linked to dermatitis can be regulated by CBD, hence alleviating symptoms like anxiety and depression as well.6, 8, 16

Diabetic Ulcer

Ulceration is a widespread development in diabetic patients, caused by the neuropathic and vascular complications. Nerve damage from diabetes can numb the feeling entirely from the foot or leg, leaving the patient without protective sensations that would otherwise signal a warning when injured. This can lead to skin loss, blisters and chronic ulcerations.

Previous research has shown that the clinical endocannabinoid deficiency in diabetes mellitus responds to CBD administration. High glucose-induced endothelial cell inflammatory response in the vascular system, can be reduced using CBD since it promotes vasodilation and improves perfusion. These properties of CBD along with its antibacterial capabilities support its viability as a treatment for diabetic ulcers.3, 17

Scleroderma

Scleroderma is not contagious, infectious, cancerous or malignant; it is a chronic disease classified as a systemic autoimmune disorder. Symptoms of The disease develops dermatologic aggravations that cause hardening of the skin and tissues. The symptoms include pain and fatigue mostly due to changes in the oxygen flow and unusual immunological responses. Scleroderma is an idiopathic autoimmune clinical endocannabinoid deficiency, which affects both CB1 and CB2 receptors. Skin elasticity and the dermatological aggravations can both be alleviated by the therapeutic administration of cannabidiol. Therefore, CBD can relieve the severity and discomfort of scleroderma.19

Skin Cancer

Most skin cancers are a locally damaging malignant growth of the skin. They arise from the cells of the epidermis, the superficial layer of the skin. Unlike cutaneous malignant melanoma, the vast majority of these sorts of skin cancers rarely metastasize and become fatal. The three principal types of skin cancer are:

  1. Basal cell carcinoma: the most common form of skin cancer.
  2. Squamous cell carcinoma: originates from skin cells.
  3. Melanoma: it is the less common form of skin cancer but also the most serious, and develops from melanocytes the pigment-producing skin cells.

Skin malignancies are acquired and idiopathic autoimmune clinical endocannabinoid deficiency. Therapeutic administration of CBD shows encouraging effects in triggering malignant cell death, repressing tumor growth and metastasis to visceral organs. Cancerous cell death can be further expedited through enhancing the autophagy process using CBD. Autophagy is the process that removes cellular waste. Conclusive research supports the anti-tumoral, anti-bacterial and analgesic effects of CBD oil and its effectiveness in skin cancer treatment.2, 5, 9, 10, 11, 13-15, 18

References:

  1. Russo E. B, Neuro Endocrinol Lett. 2004 Feb-Apr;25(1-2):31-9. Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? Available at https://www.ncbi.nlm.nih.gov/pubmed/15159679
  2. Gertsch, J. (2017) Cannabimimetic phytochemicals in the diet – an evolutionary link to food selection and metabolic stress adaptation?. British Journal of Pharmacology, 174: 1464–1483, available at https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/bph.13676
  3. Gruden, G., Barutta, F., Kunos, G., and Pacher, P. (2016) Role of the endocannabinoid system in diabetes and diabetic complications. Br J Pharmacol, 173: 1116–1127, available at https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/bph.13226
  4. Scarabino, T., Salvolini, U. Atlas of Morphology and Functional Anatomy of the Brain. Springer-Verlag Berlin Heidelberg, (2006).
  5. Roger G. Pertwee, Targeting the endocannabinoid system with cannabinoid receptor agonists: pharmacological strategies and therapeutic possibilities, Phil. Trans. R. Soc. B 2012 367 3353-3363; available at http://rstb.royalsocietypublishing.org/content/367/1607/3353.long
  6. George W. Booz, Cannabidiol as an emergent therapeutic strategy for lessening the impact of inflammation on oxidative stress, Free Radical Biology and Medicine, Volume 51, Issue 5, 2011, Pages 1054-1061, ISSN 0891-5849, available at: http://www.sciencedirect.com/science/article/pii/S0891584911000116
  7. Smith SC, Wagner MS. Clinical endocannabinoid deficiency (CECD) revisited: can this concept explain the therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? Neuro Endocrinol Lett. 2014; 35(3): 198 – 201. Available at https://www.ncbi.nlm.nih.gov/pubmed
  8. Devinsky, O et al. Cannabidiol: Pharmacology and potential therapeutic role in epilepsy and other neuropsychiatric disorders. Epilepsia 55, 791-802 (2014),  available at https://doi.org/10.1111/epi.12631
  9. Baron, E. P. (2015), Comprehensive Review of Medicinal Marijuana, Cannabinoids, and Therapeutic Implications in Medicine and Headache: What a Long Strange Trip It’s Been …. Headache: The Journal of Head and Face Pain, 55: 885-916. Available at https://doi.org/10.1111/head.12570
  10. Macpherson, T., Armstrong, J.A., Criddle, D.N. et al. In Vitro Cell.Dev.Biol.-Animal (2014) 50: 417. Available at https://doi.org/10.1007/s11626-013-9719-9
  11. McAllister, S.D., Soroceanu, L. & Desprez, PY. J Neuroimmune Pharmacol (2015) 10: 255. Available at https://doi.org/10.1007/s11481-015-9608-y
  12. Fitzcharles, MA., Baerwald, C., Ablin, J. et al. Schmerz (2016) 30: 47. Available at https://doi.org/10.1007/s00482-015-0084-3
  13. Robert Ramer, Jutta Merkord, Helga Rohde, Burkhard Hinz, Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1, Biochemical Pharmacology, Volume 79, Issue 7, 2010, Pages 955-966, ISSN 0006-2952, available at https://doi.org/10.1016/j.bcp.2009.11.007
  14. Ramer, R., Rohde, A., Merkord, J. et al. Pharm Res (2010) 27: 2162. Available at https://doi.org/10.1007/s11095-010-0219-2
  15. Robert Ramer, Katharina Bublitz, Nadine Freimuth, Jutta Merkord, Helga Rohde, Maria Haustein, Philipp Borchert, Ellen Schmuhl, Michael Linnebacher, and Burkhard Hinz, The FASEB Journal 2012 26:4, 1535-1548, available at https://doi.org/10.1096/fj.11-198184
  16. Wilkinson, Jonathan D. et al. Cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis, Journal of Dermatological Science , Volume 45 , Issue 2 , 87 – 92, available at https://doi.org/10.1016/j.jdermsci.2006.10.009
  17. Rajesh, M., Mukhopadhyay, P., Bátkai, S., Haskó, G., Liaudet, L., Drel, V. R., … Pacher, P. (2007). Cannabidiol attenuates high glucose-induced endothelial cell inflammatory response and barrier disruption. American Journal of Physiology. Heart and Circulatory Physiology, 293(1), H610–H619. Available at http://doi.org/10.1152/ajpheart.00236.2007
  18. Armstrong, Jane L. et al. Exploiting Cannabinoid-Induced Cytotoxic Autophagy to Drive Melanoma Cell Death, Journal of Investigative Dermatology, Volume 135, Issue 6, 1629 – 1637, available at https://doi.org/10.1038/jid.2015.45

Del Río, C., Navarrete, C., Collado, J. A., Bellido, M. L., Gómez-Cañas, M., Pazos, M. R., … Muñoz, E. (2016). The cannabinoid quinol VCE-004.8 alleviates bleomycin-induced scleroderma and exerts potent antifibrotic effects through peroxisome proliferator-activated receptor-γ and CB2 pathways. Scientific Reports, 6, 21703. Available at http://doi.org/10.1038/srep21703

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