question: Why are scars more sensitive to pain than other skin?
comment: Scars don't have to be painful. You get destruction and remodeling of all tissue when you have an injury, including nerve tissue. Sometimes this tissue grows back in a way that can send back more pain signals for painful stimuli or even send back pain for nonpainful stimuli (hyperalgesia vs allodynia)
passages: Skin scars occur when the dermis (the deep, thick layer of skin) is damaged. Most skin scars are flat and leave a trace of the original injury that caused them. 
  
  Wounds allowed to heal secondarily tend to scar worse than wounds from primary closure.
  
  Section::::Pathophysiology.:Collagen synthesis.
   Individuals suffering autoimmune disorders such as systemic lupus erythematosus may have an increased incidence of developing SCARs. While the cause for this possible predilection has not been determined, the altered immune system and the excessive production of cytokines occurring in these disorders could be contributing factors.
  
  Section::::Pathophysiology.:Effectors of tissue injury.
   Another major component of the ECM is hyaluronic acid (HA), a glycosaminoglycan. It is known that fetal skin contains more HA than adult skin due to the expression of more HA receptors. The expression of HA is known to down-regulate the recruitment of inflammatory cytokines interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-α); since fetal wounds contain a reduced number of pro-inflammatory mediators than adult wounds it is thought that the higher levels of HA in the fetal skin aid in scar free healing.
   Section::::Fetal vs adult healing in humans.:Immune system cells and inflammatory response.
  
  One of the major differences between embryonic scar-free healing wounds and adult scar-forming wounds is the role played by the cells of the immune system and the inflammatory response.
  
  Table 1: Summary of the major differences identified between fetal and adult wound healing.
   Section::::Pathophysiology.:T cell receptors.
  
  Due to gene editing. the number of diverse T cell receptors expressed is estimated to be as high as 10 trillion. This has made it difficult to identify specific T cell receptor types that are uniquely associated with the development of SCARs. One study, however, identified the preferential presence of the TCR-V-b and complementarity determining region 3 in T cell receptors found on the T cells in the blisters of patients with allopurinol-induced SCARs. This finding is compatible with the notion that specific types of T cell receptors are involved in the development of specific drug-induced SCARs.
   Nociceptive pain may also be classed according to the site of origin and divided into "visceral", "deep somatic" and "superficial somatic" pain. Visceral structures (e.g., the heart, liver and intestines) are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull. "Deep somatic" pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Examples include sprains and broken bones. "Superficial" pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.
   Proteins and cell surface receptors found in the ECM differ in fetal and adult wound healing. This is due to the early up regulation of cell adhesion proteins such as fibronectin and tenascin in the fetus. During early gestation in the fetal wounds of rabbits, the production of fibronectin occurs around 4 hours after wounding, much faster than in adult wounds where expression of fibronectin does not occur until 12 hours post wounding. The same pattern can be seen in the deposition of tenascin. It is this ability of the fetal fibroblast to quickly express and deposit fibronectin and tenascin, which ultimately allows cell migration and attachment to occur, resulting in an organised matrix with less scarring.
   The tissue injury in SCARs is initiated principally by CD8 or CD4 T cells. Once drug-activated, these lymphocytes elicit immune responses to self tissues that can result in SCARs drug reactions by mechanisms which vary with the type of disorder that develops. Salient elements mediating tissue injury for each type of disorder include:
   Section::::Scar free healing in nature.
   SCARs are here considered as a group focusing on the similarities and differences in their pathophysiologies, clinical presentations, instigating drugs, and recommendations for drug avoidance. Further details on these syndromes can be found on their individual Wikipedia pages.
  
  Section::::Types.
  
  Section::::Types.:SJS, TEN, and SJS/TEN.
   BULLET::::- Foreign bodies. Sharp, small foreign bodies can penetrate the skin leaving little surface wound but causing internal injury and internal bleeding. For a glass foreign body, "frequently, an innocent skin wound disguises the extensive nature of the injuries beneath". First-degree nerve injury requires a few hours to a few weeks to recover. If a foreign body passes by a nerve and causes first-degree nerve injury during entry, then the sensation of the foreign body or pain due to internal wounding may be delayed by a few hours to a few weeks after entry. A sudden increase in pain during the first few weeks of wound healing could be a sign of a recovered nerve reporting internal injuries rather than a newly developed infection.
   When the general visceral sensory fiber is simulated, the central nervous system does not clearly discern whether the pain is coming from the body wall or from the viscera, so it perceives the pain as coming from somewhere on the body wall, e.g. left arm/hand pain, jaw pain.
  
  So the pain is "referred to" the related dermatomes of the same spinal segment.
   BULLET::::- In "central sensitization," nociceptive neurons in the dorsal horns of the spinal cord become sensitized by peripheral tissue damage or inflammation. This type of sensitization has been suggested as a possible causal mechanism for chronic pain conditions. The changes of central sensitization occur after repeated trials to pain. Research from animals has consistently shown that when a trial is repeatedly exposed to a painful stimulus, the animal’s pain threshold will change and result in a stronger pain response. Researchers believe that there are parallels that can be drawn between these animal trials and persistent pain in people. For example, after a back surgery that removed a herniated disc from causing a pinched nerve, the patient may still continue to “feel” pain. Also, newborns who are circumcised without anesthesia have shown tendencies to react more greatly to future injections, vaccinations, and other similar procedures. The responses of these children are an increase in crying and a greater hemodynamic response (tachycardia and tachypnea).
   Nociceptive pathways are pathways in the brain that send and receive pain signals and are responsible for how we perceive pain. They develop before a baby is born and continue to develop during the critical period of development. It was once thought that because infants’ nociceptive pathways in the brain were still developing, they could not feel pain. However, infants "can" feel pain and infant surgeries providing early pain experiences can alter the brain’s tolerance for pain later so by increasing number of A fibers and C fibers—two types of pain receptors—located in the area where injury occurred and by reducing pain tolerance in the areas where incision has occurred. This reduction in pain tolerance is seen in male rats even when they are adolescents. In those rats, the area of their brain where an incision was made as an infant remains hypersensitive to pain thereafter. This effect was not seen as prominently in female rats.
   Reparation of tissue in the mammalian fetus is radically different than the healing mechanisms observed in a healthy adult. During early gestation fetal skin wounds have the remarkable ability to heal rapidly and without scar formation. Wound healing itself is a particularly complex process and the mechanisms by which scarring occurs involves inflammation, fibroplasia, the formation of granulation tissue and finally scar maturation. Since the observation of scar free healing was first reported in the early fetus more than three decades ago, research has focused intently on the underlying mechanisms which separate scarless fetal wound repair from normal adult wound healing.
   Section::::Clinical significance.:Injury.:Penetrating wounds.
  
  Most penetration wounds require immediate treatment and are not as easy to repair. For example, a deep knife wound to the brachial plexus could damage and/or sever the nerve. According to where the cut was made, it could inhibit action potentials needed to innervate that nerve's specific muscle or muscles.
  
  Section::::Clinical significance.:Injury.:Injuries during birth.
   The fibroblast involved in scarring and contraction is the myofibroblast, which is a specialized contractile fibroblast. These cells express α-smooth muscle actin (α-SMA).
  
  The myofibroblasts are absent in the first trimester in the embryonic stage where damage heals scar free; in small incisional or excision wounds less than 2 mm that also heal without scarring; and in adult unwounded tissues where the fibroblast in itself is arrested; however, the myofibroblast is found in massive numbers in adult wound healing which heals with a scar.
   The nerves of young babies respond more readily to noxious stimuli, with a lower threshold to stimulation, than those of adults. A baby's threshold for sensitization is also substantially decreased, whilst the process involves a much larger area of sensitization with each trauma. The neural pathways that descend from the brain to the spinal cord are not well developed in the newborn, resulting in the ability of the central nervous system to inhibit nociception being more limited than in the adult.
   Peripheral injuries trigger complex changes in the central nociceptive system which can lead to central sensitization that enhances the sensitivity and responsiveness of the brain regions involved in sensory processing. In some cases, these physiological responses progress to neuropathic centralized pain.
  
  Section::::Treatments.
   Section::::Nature of the scars.
  
  Because "Mensur" swords are wielded with one hand and most fencers are right-handed, "Mensur" scars were usually targeted to the left profile, so the right profile appeared untouched. Experienced fencers, who had fought many bouts, often accumulated an array of scars. A duelist who died in 1877 "...fought no less than thirteen duels but had 137 scars on head, face and neck".
   There are two types of nerve fibre relevant to pain in amphibians. Group C nerve fibres are a type of sensory nerve fibre which lack a myelin sheath and have a small diameter, meaning they have a low nerve conduction velocity. The suffering associated with burns, toothaches, or crushing injury are caused by C fibre activity. A-delta fibres are another type of sensory nerve fibre, however, these are myelinated and therefore transmit impulses faster than non-myelinated C fibres. A-delta fibres carry cold, pressure and some pain signals, and are associated with acute pain that results in "pulling away" from noxious stimuli.
   In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 "Science" article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt.
   BULLET::::- Pattern II : The scar presents T-cells and macrophages around blood vessels, with preservation of oligodendrocytes, as before, but also signs of complement system activation can be found. Though this pattern could be considered similar to damage seen in NMO, some authors report no AQP4 damage in pattern II lesions
   A painful facial expression is one way in which the experience of pain is communicated from one individual to another. One study aimed to measure test subject’s related brain activity and facial muscle activity when they watched video clips of a variety of facial expressions including neutral emotion, joy, fear, and pain. The study found that when a subject is shown a painful facial expression, their late positive potential (LPP) is increased during the time period of 600–1000ms after the initial exposure of the stimulus. This increase in LPP for painful facial expressions was higher than the increase caused by other emotional expressions. 
   The appearance and nature of the wound varies with the type of weapon used and the location of the injury, and may present as a laceration, abrasion, contusion or bone fracture. Where a victim has time to raise hands or arms before being shot by an assailant, the injury may also present as a gunshot wound. Severe laceration of the palmar surface of the hand or partial amputation of fingers may result from the victim grasping the blade of a weapon during an attack. In forensic pathology the presence of defense wounds is highly indicative of homicide and also proves that the victim was, at least initially, conscious and able to offer some resistance during the attack.
  
raw_presuppositions: Scars are always more sensitive to pain than other skin. Scars are more sensitive to pain than other skin.
raw_corrections: Sometimes scars are more sensitive to pain due to the way tissue grows back, however not all scars are painful. Scars don't have to be painful, it depends on the way the scar tissue grows back.