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 Table of Contents  
REVIEW ARTICLE
Year : 2017  |  Volume : 7  |  Issue : 2  |  Page : 129-134

Photobiomodulation and oral wound healing


Department of Oral Pathology, Karpaga Vinayaga Institute of Dental Sciences, Kanchipuram, Tamil Nadu, India

Date of Web Publication28-Dec-2017

Correspondence Address:
Dr. S Marytresa Jeyapriya
Department of Oral Pathology, Karpaga Vinayaga Institute of Dental Sciences, Palayanoor, Kanchipuram, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijmd.ijmd_60_17

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  Abstract 


Wounds can be classified into different types based on the etiology, clinical presentation, degree of contamination, and the extent of involvement of overlying skin. Wound healing is a complex, dynamic, well-orchestrated biological process that plays a vital role in the survival of humans. Both wounding and wound healing may occur in any tissue or organ of the body. In adults, wound healing commences as a cascade and includes the following phases: 1. hemostasis, 2. inflammation, 3. proliferation, 4. angiogenesis, 5. re-epithelialization, and 6. cross linking of collagen. Photobiomodulation (PBM) or low level laser therapy employs light energy to produce biological cell response and to restore cell function. It uses nonionizing light sources such as light emitting diodes and lasers, in the visible and infrared spectrum, and it is found to elicit numerous therapeutic benefits such as immunomodulation, promotion of wound healing, and rapid regeneration of tissues. This review aims to explore the molecular mechanisms of PBM and its role in wound healing. Further studies on the molecular mechanisms of PBM and their pathways can preclude promising clinical interventions for wound care.

Keywords: Low-level laser therapy; oral wound healing; photobiomodulation therapy; wound healing; wounds


How to cite this article:
Vinesh E, Jeyapriya S M, Kumar M S, Arunachalam M. Photobiomodulation and oral wound healing. Indian J Multidiscip Dent 2017;7:129-34

How to cite this URL:
Vinesh E, Jeyapriya S M, Kumar M S, Arunachalam M. Photobiomodulation and oral wound healing. Indian J Multidiscip Dent [serial online] 2017 [cited 2019 Jul 21];7:129-34. Available from: http://www.ijmdent.com/text.asp?2017/7/2/129/221773


  Introduction Top


A wound is defined as damage or disruption to the normal anatomical structure and function.[1],[2]


  Classification of Wounds Top


Clinically, wounds can be classified into three types,[2] namely acute wounds, chronic wounds, and complicated wounds [Table 1].
Table 1: Classification of wounds

Click here to view


Acute wounds

These wounds repair themselves and follow a normal, timely, and orderly healing course (from 5 to 10 days). They may occur as a result of a surgical procedure or trauma.[1],[3]

Chronic wounds

These type of wounds fail to repair in an orderly, timely manner and do not follow the normal course of healing process.[1],[4] The healing is incomplete, and relapse frequently occurs.[1],[5] They may occur as a result of burns, vasculitis, and arterial/venous insufficiency.[5]

Complicated wounds

A complicated wound is said to be a combination of an infection and a tissue defect.[6] In these types of wounds, infection becomes a serious threat to the wound.[6]

According to etiology, wounds can be classified into

  • Contusions
  • Abrasions
  • Avulsions
  • Lacerations
  • Cuts
  • Stab wounds
  • Shot wounds
  • Burns.[1],[3],[6],[7]


Based on the degree of contamination, wounds can be classified into

  • Aseptic wounds
  • Contaminated wounds
  • Septic wounds.[5],[7],[8]


Wounds can also be classified into

  • Open wounds: wounds where the skin is damaged and the underlying tissue is exposed
  • Closed wounds: wounds where the underlying tissue is traumatized with the skin intact.[5],[6],[8],[9]


Wound healing

Wound healing is a complex, precisely regulated, dynamic, well-orchestrated biological process that plays a critical role in the survival of humans.[7],[9],[10],[11],[12],[13],[14]

Both wounding and wound healing may occur in any tissue or organ of the body.[2]


  Phases of Wound Healing Top


In adults, wound healing commences as a cascade and includes the following phases [Table 2]:
Table 2: Phases of wound healing and cellular events

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  1. Hemostasis
  2. Inflammation
  3. Proliferation
  4. Angiogenesis
  5. Re-epithelialization
  6. Cross-linking of collagen.[15]


Following a wound, a blood clot forms as a result of activated coagulation pathways. The clot releases cytokines and vascular endothelial growth factor (VEGF).[16] Neutrophils are attracted by these secreted chemokines, and they migrate into the wound. The neutrophils release proteolytic enzymes and destroy the invading microorganisms, and they also secrete proteases and reactive oxygen species.

Macrophages infiltrate into the area and release cytokines, activate leucocytes, induce apoptosis, and clear the apoptotic cells. Subsequently, the macrophages stimulate keratinocytes, fibroblasts and induce angiogenesis.[17],[18] The above events are followed by the migration of T lymphocytes into the wound area. It is believed that CD4+ cells promote wound healing whereas CD8+ cells inhibit wound healing.[19],[20] During wound healing, dendritic epidermal T cells when activated produce fibroblast growth factor 7 (FGF– 7), chemokines, and other cytokines that enhance keratinocyte proliferation and regulate inflammation.[21]

The inflammatory phase is followed and overlapped by proliferative phase. It includes re-epithelialization. The subjacent fibroblasts and endothelial cells orchestrate angiogenesis, synthesis of collagen, and granulation tissue formation in the site of the wound. The fibroblasts begin to synthesize extracellular matrix (ECM). In the final remodeling phase, the newly formed capillaries regress and the ECM returns to its normal architecture. Contractile fibroblasts mediate the contraction of the wound.[22],[23]

Oral wound healing

Wound healing in the oral cavity is a complex process and can be attributed to the complex interactions between oral keratinocytes, ECM of the oral mucous membrane, bacteria, saliva, and gingival crevicular fluid. Integrins such as α2 β1, α3 β1, αvβ5, αvβ6, vitronectin, tenascin–C, transforming growth factor β and wound fibroblasts, thrombospondin and secreted protein rich in cysteine/osteonectin play a vital role in the physiology of oral wound healing. As a result of these myriad interactions, oral mucosal wounds heal more rapidly with less scarring than dermal wounds.[14],[24],[25]

Biophysical therapies for wound healing

Over the past few decades, several biophysical therapies have been employed to promote wound healing. A few commonly used biophysical interventions include microcurrent, electromagnetic fields, ultrasound, pressure, and light therapies.[26] In 1968, Professor Endre Mestre demonstrated that high power lasers had the ability to rapidly heal experimental skin defects, diabetic ulcers, and infected wounds. This experimental research led to the discovery and development of photobiomodulation (PBM).[27]

Photobiomodulation

PBM or low-level laser therapy (LLLT) employs light energy to produce biological cell response and to restore cell function.[28] PBM, a form of phototherapy, uses nonionizing light sources such as light emitting diodes and lasers in the visible and infrared spectrum and it is found to elicit numerous therapeutic benefits such as immunomodulation, promotion of wound healing, and rapid regeneration of tissues. PBM is based on Arndt–Schulz law. According to the law, a weak stimulus improves a specific biological function, and a stronger stimulus elevates the effect further. Once a peak response is attained, further increase in stimulus results in a negative response.[26],[29]

PBM, when applied to pathology, promotes tissue regeneration, reduces inflammation, and relieves pain. PBM is considered to elicit a nonablative, nonthermal, photochemical, therapeutic effect in biological tissues.[29]


  Molecular Mechanisms of Photobiomodulation Top


Based on the time period from intervention, PBM mechanisms can be classified into the following two phases [Figure 1]:
Figure 1: Molecular mechanisms of photobiomodulation

Click here to view


  1. Primary phase
  2. Secondary phase.


Primary phase events are of two types

  1. Direct events (occur as a result of interaction of light energy with tissues)
  2. Indirect events (immediately follow direct events).


The primary phase events are transient, critical, and subsequently elicit biological tissue responses that lead to the secondary phase events.[26]

According to the 1st law of photobiology, in order for PBM to be effective, the photos by generated by PMB therapy must be absorbed by molecular photoacceptors (chromophores) in the biological tissue.[30]

A chromophore is a molecule (or a part of a molecule) which imparts a specific color to the biological compound of which it is a component, for example, hemoglobin and cytochrome Coxidase (CCO).[29],[31] Some examples of biological, mammalian chromophores are 7 dehydrocholesterol, rhodopsin, photopsin, cytochrome oxidase, flavins, nicotinamide adenine dinucleotide phosphate, and so on. The “optical window” of the human tissue ranges from 650 nm to 1200 nm and within this spectrum, the tissue penetration of light is maximized.[29] This necessitates the use of LLLT in the range of red and infrared light (600–1100 nm) in humans.[32]

Primary phase events

These events occur within a few seconds/minutes of treatment and are photochemical and photophysical in nature.[26]

Direct events

Two distinct types of direct events can be elicited by LLLT:

In the first type, once LLLT is administered, the light energy is absorbed by a chromophore (in the biological tissue). A redox reaction results and electrons are released. Reactive oxygen species (ROS) such as hydrogen peroxide, superoxide, and hydroxyl radicals are released and they initiate numerous biological responses.[33]

In the second type of direct events, the LLLT administered results in change in conformational structure of biomolecules and favor its physiological function.[34]

Both the events act as “sensors” and they occur within fractions of seconds of LLLT application.

Indirect events

The primary direct events are followed by a cascade of sequential, biological events, which occur within seconds to minutes of PBM.[26]


  Role of Photobiomodulation-Generated Reactive Oxygen Species Top


The ROS (superoxide, O2) generated during the primary direct events reacts with nitric oxide (NO, produced by interaction of LLLT with nitrogen) to form ONOO (peroxynitrite) which causes biological responses.[35] PBM-generated ROS can produce modulation of antioxidants and induce protein modification and oxidative stress-mediated gene expression and lead to transcription of gene products.[36] A classic example of protein modification is production of disulfide bonds by cysteine residues. This leads to alteration in the structure and functions of enzymes, notably phosphatases. Inactivated, structurally altered phosphatases can elicit transcriptional changes.[37]

ROS also modulates mitochondrial respiration and activates NF-κB signaling pathway.[38] ROS tends to activate Src, a nonreceptor tyrosine kinase, which in turn enhances cell proliferation, attachment, migration, and cell survival.[39] PBM-generated ROS interacts with methionine 253 on latent TGF-β1 and leads to its activation.[40] This in turn contributes to oral mucosal wound healing.[26]


  Role of Cytochrom C Oxidase Top


Another biological photoacceptor CCO absorbs LLLT and disrupts electron transfer process, resulting in increase in ATP production.[41] This, in turn, modulates a spectrum of biological effects that include synthesis/activation of DNA, proteins, RNA, enzymes and also aids in the repair and regeneration of cells and tissues.[26]

Photoabsorption by CCO also leads to dissociation of NO from Fe/Cu redox centres.[42],[43] The NO released leads to vasodilation and also activates Ca-sensitive K (kc) channels.[44] Dissociated NO promotes wound healing by enhancing keratinocyte proliferation, migration of endothelial cells, lumenization, macrophage function, vasodilation, and stem cell differentiation.[26]

Secondary phase events

The primary phase events are followed by induced secondary phase pathways that occur hours to days after PMB therapy. These secondary phase responses have a long-term effect on biological tissue. The secondary phase events in wound healing include signaling of autocrine/paracrine hormones, migration, proliferation and differentiation of cells, angiogenesis, and synthesis of ECM.[26]

Secondary phase events and their relation to the phases of wound healing

Hemostasis

PBM stimulates platelet aggregation and activates coagulation pathways and thus plays a critical role in hemostasis.

Inflammation

PBM is known to promote proliferation of mast cells and also plays an active role in the degranulation of mast cells.[45]

PBM therapy has direct effects on pro-inflammatory factors and anti-inflammatory factors such as interleukin [IL]-1, IL-8, COX 1 and COX 2.[46],[47] The inflammatory phase of wound healing is characterized by clearing of debris and migration of keratinocytes and fibroblasts.[26] PBM therapy modulates inflammation and also regulates immune microenvironment. It induces cytokines and growth factors such as basic fibroblast growth factor (FGF), FGF-1, FGF-2, transforming growth factor-β, and VEGF over a period of hours to days after exposure to therapy.[48] These factors in turn play a key role in wound healing by inducing proliferation of keratinocytes, proliferation and migration of fibroblasts, wound contraction, inflammation, neovascularization, matrix synthesis, and remodeling.[49],[50],[51]

Proliferation

PBM induces proliferation of oral keratinocytes, fibroblasts, chondrocytes, and also ECM synthesis.[52]

Angiogenesis

PBM aids in neovascularization, angiogenesis and improves the tensile strength of wounded tissues and restores functional structure of repaired tissues. It thus stimulates reorganization, repair, and wound healing.[53]

Re-epithelialization

PBM tends to aid in enhancing epithelialization and improves wound healing especially in gingivectomy and gingivoplasty wounds.[54]

Downstream cellular and tissue effects of photobiomodulation

In the cellular level, PBM acts on mitochondria and increases ATP synthesis, RNA and protein synthesis and membrane potential.[29],[55]

NO produced by the mitochondria binds to COX (the primary photo acceptor for mammalian cells) and inhibits respiration. LLLT dissociates NO from COX and reverses inhibition of respiration.[42],[56],[57] NO can also be released by LLLT from nitrosylated hemoglobin and nitrosylated myoglobin. This may in turn result in vasodilation.[29],[58]

PBM prevents cellular apoptosis and enhances cell proliferation, migration, and adhesion in keratinocytes.[29],[59] PBM also stimulates neovascularization, promotes angiogenesis, increases collagen synthesis, and promotes healing of wounds.[60],[61]


  Conclusion Top


Numerous randomized controlled trials have proved that the use of PBM contributes significantly to wound healing. The primary phase events and the secondary phase events in PBM therapy play a critical role in healing of wounds by photodissociation of ROS and CCO. These dissociated intermediates play an active role in each phase of the wound healing process. In the cellular level, PBM increases synthesis of ATP and RNA. In addition, PBM prevents apoptosis, enhances angiogenesis, and induces synthesis of ECM. All these events exert a synergistic influence on wound healing. Further studies on the molecular mechanisms of PBM and their pathways can preclude promising clinical interventions for wound care.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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