The Effect of Thermal Heat and Cold Applicatıons On Inflammation: A Review Of Current Literature
INFLAMMATION, Tunçsiper B. & Mete B.D., Editör, Gece Kitaplığı Yayınevi, Ankara, ss.319-344, 2022
- Yayın Türü: Kitapta Bölüm / Mesleki Kitap
- Basım Tarihi: 2022
- Yayınevi: Gece Kitaplığı Yayınevi
- Basıldığı Şehir: Ankara
- Sayfa Sayıları: ss.319-344
- Editörler: Tunçsiper B. & Mete B.D., Editör
- Ankara Yıldırım Beyazıt Üniversitesi Adresli: Evet
Özet
Healing is a complicated process that consists of three overlapping
phases: 1) inflammation, 2) proliferation and 3) maturation (Li, Chen,
& Kirsner, 2007). When tissue damage occurs due to bacteria, trauma,
chemicals, temperature or any other event, a large number of substances
are released from the damaged tissue. The release of the substance causes
dramatic secondary changes in the undamaged tissue near the injured area.
This whole complex of tissue changes is called inflammation (Hall & Hall,
2021). In other words, inflammation can be defined as a process that damages
cells or tissues at the beginning of the injury. However, inflammation and
healing are intertwined defence mechanisms of the body. If there is no
inflammation, the healing process cannot be commenced. With these repair
mechanisms, the inflammatory factor is destroyed and removed from the
injured area. Then, the damaged tissue is repaired by limiting inflammation
(M.H. Cameron, 2017; Kuralay & Çavdar, 2006). Cytokines are chemical
mediators that mediate the inflammatory tissue response. Cytokines
originating from mononuclear phagocytes are called monokine, cytokines
originating from lymphocytes are called lymphokines, and cytokines
originating from leukocytes are called interleukins. Tumour necrosis factor
(TNF) is one of the main mediators of the acute inflammatory response.
IL-1 acts together with TNF for the response against inflammation, both
are proinflammatory cytokines. IL-10 plays a role in the control of innate
immune reactions and cellular immunity and is an anti-inflammatory
cytokine that inhibits macrophage activation (Hall & Hall, 2021). The
inflammatory phase generally takes several days. However, there is no
consensus about the duration of the inflammation. The durations reported
have ranged between 4 and 6 days (Garrett Jr, 1990; Kellett, 1986). The
disagreement may be associated with individual differences and injury
types (M.H. Cameron, 2017).