Ogawa R
International journal of molecular sciences. Date of publication 2017 Mar 10;volume 18(3):.
1. Int J Mol Sci. 2017 Mar 10;18(3). pii: E606. doi: 10.3390/ijms18030606.
Keloid and Hypertrophic Scars Are the Result of Chronic Inflammation in the
Reticular Dermis.
Ogawa R(1).
Author information:
(1)Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical
School Hospital, Tokyo 113-8603, Japan. r.ogawa@nms.ac.jp.
Keloids and hypertrophic scars are caused by cutaneous injury and irritation,
including trauma, insect bite, burn, surgery, vaccination, skin piercing, acne,
folliculitis, chicken pox, and herpes zoster infection. Notably, superficial
injuries that do not reach the reticular dermis never cause keloidal and
hypertrophic scarring. This suggests that these pathological scars are due to
injury to this skin layer and the subsequent aberrant wound healing therein. The
latter is characterized by continuous and histologically localized inflammation.
As a result, the reticular layer of keloids and hypertrophic scars contains
inflammatory cells, increased numbers of fibroblasts, newly formed blood vessels,
and collagen deposits. Moreover, proinflammatory factors, such as interleukin
(IL)-1α, IL-1β, IL-6, and tumor necrosis factor-α are upregulated in keloid
tissues, which suggests that, in patients with keloids, proinflammatory genes in
the skin are sensitive to trauma. This may promote chronic inflammation, which in
turn may cause the invasive growth of keloids. In addition, the upregulation of
proinflammatory factors in pathological scars suggests that, rather than being
skin tumors, keloids and hypertrophic scars are inflammatory disorders of skin,
specifically inflammatory disorders of the reticular dermis. Various external and
internal post-wounding stimuli may promote reticular inflammation. The nature of
these stimuli most likely shapes the characteristics, quantity, and course of
keloids and hypertrophic scars. Specifically, it is likely that the intensity,
frequency, and duration of these stimuli determine how quickly the scars appear,
the direction and speed of growth, and the intensity of symptoms. These
proinflammatory stimuli include a variety of local, systemic, and genetic
factors. These observations together suggest that the clinical differences
between keloids and hypertrophic scars merely reflect differences in the
intensity, frequency, and duration of the inflammation of the reticular dermis.
At present, physicians cannot (or at least find it very difficult to) control
systemic and genetic risk factors of keloids and hypertrophic scars. However,
they can use a number of treatment modalities that all, interestingly, act by
reducing inflammation. They include corticosteroid injection/tape/ointment,
radiotherapy, cryotherapy, compression therapy, stabilization therapy,
5-fluorouracil (5-FU) therapy, and surgical methods that reduce skin tension.
DOI: 10.3390/ijms18030606
PMCID: PMC5372622
PMID: 28287424 [Indexed for MEDLINE]
