{"id":998,"date":"2024-02-18T21:03:36","date_gmt":"2024-02-19T02:03:36","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&p=998"},"modified":"2026-01-03T16:16:56","modified_gmt":"2026-01-03T21:16:56","slug":"section-3-cell-proliferation-and-tissue-regeneration-and-repair-2","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/section-3-cell-proliferation-and-tissue-regeneration-and-repair-2\/","title":{"raw":"Cell Damage, Acute and Chronic Inflammation, Blood Test Serum Markers, Cell Proliferation, Tissue Repair and Possible Complications","rendered":"Cell Damage, Acute and Chronic Inflammation, Blood Test Serum Markers, Cell Proliferation, Tissue Repair and Possible Complications"},"content":{"raw":"

Cell Damage<\/strong><\/h3>\r\nCells can be damaged by physical or mechanical stresses (e.g. blunt trauma, cuts, surgical incisions).\u00a0 Cells can also be damaged by pathogens (e.g. bacteria, viruses, protozoa, helminths, fungi and prions) and pathogenic enzymes and toxins.\u00a0 Cells can be damaged by lack of oxygen, waste accumulation, and excessive heat or cold temperatures.\u00a0 Auto-immune diseases and cancers can cause cellular damage.\u00a0 Cells can also be damaged by electrical burns, acids, bases, radiation, toxic endogenous or exogenous chemicals, free radicals, (e.g. Reactive Oxidative Species, HO2<\/sub>, OH*<\/sup>, O2<\/sub>*<\/sup>),\r\n\r\n \r\n

Diagnostic Tests - Blood Tests and Serum Markers\u00a0\u00a0<\/strong><\/h3>\r\nOften changes in the blood can yield diagnostice clues as to the cause or extent of cellular damage that has occurred.\r\n\r\nFor example, damaged cells release cytokines that stimulate the inflammatory response.\u00a0 As a result there is an increase in inflammatory plasma proteins<\/strong> (e.g. prothrombin, fibrinogen, C-reactive proteins, and plasminogen).\r\n\r\nIn addition to inflammatory markers, a rise in specific antibodies<\/strong> occurs during an infection, as does the concentration of complement proteins<\/strong>.\u00a0 \u00a0The proportions of WBCs can be altered as well depending on the type of infection.\u00a0 Neutrophilia<\/strong> (increased neutrophil counts) often occurs with bacterial infections.\u00a0 Eosinophilia<\/strong> (increased eosinophil counts) often occurs with helminth infections.\u00a0 Lymphocytosis<\/strong> (increases in NK, T, and B lymphocytes) occurs with viral infections\r\n\r\nDamaged cells often release cellular content that can give clues as to what types of cells have been damaged.\u00a0 For example damaged hepatocytes (liver cells) release liver enzymes<\/strong> (e.g. ALT, GGT, and AST) into the bloodstream.\u00a0 Heart cells that are damaged in a myocardial infarction release cellular proteins<\/strong> (e.g. cardiac troponin, actin, myosin and creatine kinase) into the bloodstream.\u00a0 Monitoring specific cellular enzyme and protein concentrations in the blood helps to inform the level and duration of the damage that has occurred to specific tissues in the body.\r\n\r\n \r\n

Acute Inflammation and Preparation for Healing<\/strong><\/h3>\r\nAs mentioned in previous sections, tissue damage always results in inflammation.\u00a0 The steps involved are as follows:\r\n
    \r\n \t
  1. Cells that are damaged release cellular contents (e.g. ADP, K+<\/sup>, proteins and enzymes<\/strong>) and sometimes cytokines<\/strong> which stimulates the activity of macrophages<\/strong> and mast cells<\/strong>.\u00a0 Macrophages phagocytose debris and infecting pathogens (if present) as well as release chemokines to induce the chemotaxis and recruitment of other WBCs.\u00a0 Mast cells degranulate to release pro-inflammatory cytokines (e.g. histamine, bradykinin, and prostaglandins).\u00a0 Cells that are damaged are not functional, so loss of function of this tissue will occur until healing (if possible) occurs<\/li>\r\n \t
  2. The pro-inflammatory cytokines<\/strong> bind to receptors on blood vessel walls and induce vasoconstriction as well as increased capillary permeability.\u00a0 These cytokines can also trigger nociceptors resulting in pain<\/strong> sensations.\u00a0 Leaked blood can also stimulate nociceptors.\u00a0 Activated WBCs and some infectious agents release pyrogens<\/strong> as well which may give rise to fever.<\/li>\r\n \t
  3. The resulting increase in blood flow makes the tissue warm<\/strong> and red.<\/strong>\u00a0 The increase in plasma fluid entering the tissue bed results in swelling<\/strong> and pain.\u00a0 The leaked plasma fluid contains platelets and plasma proteins that assist with the immune response (e.g. fibrinogen, complement proteins, C-reactive proteins).\u00a0 Fibrin mesh and clots help to contain the area and phagocytes remove cellular debris and any pathogens.\u00a0 There is pain or swelling in a joint, muscle or bone, it may impede movement until healing occurs.<\/li>\r\n \t
  4. The WBCs that often migrate to the area include neutrophils, eosinophils, macrophages, dendritic cells, and NK cells (Natural Killer lymphocytes.\u00a0 WBCs remove infectious agents, toxins, and debris.<\/li>\r\n \t
  5. At the same time platelets and tissues release growth factors to stimulate mitosis of replacement tissue cells.\u00a0 Fibroblasts are abundant in the connective tissue throughout the body and produce collagen to help bind tissue together.\u00a0 At this point in time, when healing has begun there are three possible outcomes.<\/li>\r\n<\/ol>\r\n

    Healing<\/strong><\/h3>\r\n
      \r\n \t
    1. Resolution:\u00a0<\/strong> It may be that the damaged cells do not die, and recover.\u00a0 In this case, the term resolution is used and leads to return to full function.<\/li>\r\n \t
    2. Regeneration:<\/strong>\u00a0 If the tissue is small and involves cell types that are readily able to regenerate, tissue stem cells will produce daughter cells through mitosis that lead to a replacement of lost tissue with the exact same types of cells.\u00a0 This is termed regeneration.\u00a0 Many types of epithelial cells, connective tissue cells, and even liver cells are very regenerative.<\/li>\r\n \t
    3. Replacement:\u00a0 <\/strong>Cardiac muscle cells, skeletal muscle cells, kidney cells, brain and spinal cord neurons and some areas of cartilage are not very regenerative.\u00a0 In the case where damage has occured to cell types that are not regenerative or if the wound or damage is signicant, it may be that an abundance of collagen and other cell types (e.g. fibroblasts) is required to replace the lost tissue forming what is known as scar tissue.\u00a0 This process is termed fibrosis<\/strong> and involves the permanent loss of functional tissue.<\/li>\r\n<\/ol>\r\nDuring the healing process, capillaries become less permeable, and blood vessel diameter returns to normal.\u00a0 WBCs become inactivated and fibrin mesh and clots are enzymatically cleaved, dissolved and removed.\u00a0 The excess fluid in the interstitial space is absorbed by lymph vessels and returned to the bloodstream.\u00a0 The signs of inflammation (redness, warmth, swelling and pain) all diminish.\r\n\r\n \r\n

      Possible Complications of Tissue Damage and Inflammation<\/strong><\/h3>\r\nPossible complications of tissue damage and inflammation include the following:\r\n
        \r\n \t
      1. Chronic Inflammation:\u00a0<\/strong> If the cause of damage is not removed (e.g. many auto-immune diseases), the perpetual damage may lead to more and more damage and activated WBCs which can cause collateral damage, delay healing and lead to fibrosis (permanent scarring and loss of functional tissue).<\/li>\r\n \t
      2. Infection:\u00a0<\/strong> If the wound is exposed to the external environment, microorganisms (even members of one's normal flora) can become opportunistic and cause infection and therefore more damage.<\/li>\r\n \t
      3. Deep ulcers:<\/strong>\u00a0 Damage to gastric mucosa can allow for gastric acids to erode underlying tissue and damage blood vessel resulting in severe and prolonged inflammation, bleeding, necrosis, infection, possible loss of functional tissue, and fibrosis.<\/li>\r\n \t
      4. Skeletal Muscle Spasms:<\/strong> can occur as a protective response to pain during sprains (damage to ligaments) and strains (damage to muscle or tendon).\u00a0 Spasms that occur in bone fractures can force movement of broken bone ends resulting in shearing of tissue.\u00a0 (Note:\u00a0 Temporary muscle spasms (e.g. charley horse) during excessive exercise are different in that the cause is thought to be not enough blood flow, cellular dehydration, and\/or electrolyte depletion).<\/li>\r\n \t
      5. Peripheral Nerve damage:<\/strong> can lead to permanent or temorary loss of sensation, paresthesias if damage is to sensory nerves and muscle weakness or paralysis if motor neurons are affected.\u00a0 If peripheral nerve cells recover, function may be regained.\u00a0 Loss of brain or spinal cord nerves is permanent and can lead to permanent losses of function - though some brain plasiticty may occur through rehabilitation.<\/li>\r\n \t
      6. Obstruction:<\/strong>\u00a0 Swelling in the esophagus can lead to problems swallowing.\u00a0 Swelling affecting the bronchioles, bronchi, or other parts of the respiratory tract can lead to problems breathing and potentially can affect gas exchange abilities of the lungs.<\/li>\r\n \t
      7. Increased I<\/span>ntrac<\/span>ranial P<\/span>ressure (ICP):<\/strong>\u00a0 Swelling in the brain or cranial meninges can lead to increased intracranial pressures which can be fatal due to the pinching off of capillaries and reduced blood flow.<\/li>\r\n \t
      8. Myositis Ossificans:<\/strong>\u00a0 This refers to the calcification that can occassionally occur within injured muscles, most commonly the arm or thigh muscles (e.g. quadriceps).\u00a0 Risk factors include deep contusions that occur with contact sports (e.g. American football).\u00a0 The pathogenesis of calcification is unclear, but is likely linked to large reserve of available calcium in skeletal muscles tissues, as well as inappropriate differentiation of local stem cells into osteoblasts.\u00a0 Prevention may be assisted by treating deep contusions promptly with RICE (Rest, Ice, Compression, and Elevation).<\/li>\r\n<\/ol>\r\n \r\n

        Chronic Inflammation<\/strong><\/h3>\r\nChronic inflammation can follow an acute episode of inflammation if the source of irritation is not entirely removed.\u00a0 It may be that the tissue continues to exposed to damage from any of the following:\u00a0 an infection (pathogen or pathogenic toxins), smoking, ingested or inhaled environmental pollutants, cancer, or chronic diseases such as diabetes, auto-immune diseases (e.g. Rheumatoid Arthritis, Systemic Lupus Erythematosus), and chronic diseases of the lungs, heart, kidneys, liver, digestive system, etc..\r\n\r\nChronic inflammation defers from acute inflammation in that there is:\r\n
          \r\n \t
        1. Less swelling and exudate<\/li>\r\n \t
        2. More angiogenesis<\/li>\r\n \t
        3. More lymphocytes, macrophages, & fibroblasts are present<\/li>\r\n \t
        4. Continued tissue destruction<\/li>\r\n \t
        5. More collagen produced \u2192 fibrous scar tissue (fibrosis)<\/li>\r\n \t
        6. Possible formations of Granulomas (=small mass of cells with a necrotic center, covered by connective tissue) which are long lasting.\u00a0 Granulomas may develop in rheumatoid arthritis and osteoarthritis, or\u00a0 around a foreign object (possibly involving an abscess), or at a site of chronic infection such as tuberculosis.<\/li>\r\n<\/ol>","rendered":"

          Cell Damage<\/strong><\/h3>\n

          Cells can be damaged by physical or mechanical stresses (e.g. blunt trauma, cuts, surgical incisions).\u00a0 Cells can also be damaged by pathogens (e.g. bacteria, viruses, protozoa, helminths, fungi and prions) and pathogenic enzymes and toxins.\u00a0 Cells can be damaged by lack of oxygen, waste accumulation, and excessive heat or cold temperatures.\u00a0 Auto-immune diseases and cancers can cause cellular damage.\u00a0 Cells can also be damaged by electrical burns, acids, bases, radiation, toxic endogenous or exogenous chemicals, free radicals, (e.g. Reactive Oxidative Species, HO2<\/sub>, OH*<\/sup>, O2<\/sub>*<\/sup>),<\/p>\n

           <\/p>\n

          Diagnostic Tests – Blood Tests and Serum Markers\u00a0\u00a0<\/strong><\/h3>\n

          Often changes in the blood can yield diagnostice clues as to the cause or extent of cellular damage that has occurred.<\/p>\n

          For example, damaged cells release cytokines that stimulate the inflammatory response.\u00a0 As a result there is an increase in inflammatory plasma proteins<\/strong> (e.g. prothrombin, fibrinogen, C-reactive proteins, and plasminogen).<\/p>\n

          In addition to inflammatory markers, a rise in specific antibodies<\/strong> occurs during an infection, as does the concentration of complement proteins<\/strong>.\u00a0 \u00a0The proportions of WBCs can be altered as well depending on the type of infection.\u00a0 Neutrophilia<\/strong> (increased neutrophil counts) often occurs with bacterial infections.\u00a0 Eosinophilia<\/strong> (increased eosinophil counts) often occurs with helminth infections.\u00a0 Lymphocytosis<\/strong> (increases in NK, T, and B lymphocytes) occurs with viral infections<\/p>\n

          Damaged cells often release cellular content that can give clues as to what types of cells have been damaged.\u00a0 For example damaged hepatocytes (liver cells) release liver enzymes<\/strong> (e.g. ALT, GGT, and AST) into the bloodstream.\u00a0 Heart cells that are damaged in a myocardial infarction release cellular proteins<\/strong> (e.g. cardiac troponin, actin, myosin and creatine kinase) into the bloodstream.\u00a0 Monitoring specific cellular enzyme and protein concentrations in the blood helps to inform the level and duration of the damage that has occurred to specific tissues in the body.<\/p>\n

           <\/p>\n

          Acute Inflammation and Preparation for Healing<\/strong><\/h3>\n

          As mentioned in previous sections, tissue damage always results in inflammation.\u00a0 The steps involved are as follows:<\/p>\n

            \n
          1. Cells that are damaged release cellular contents (e.g. ADP, K+<\/sup>, proteins and enzymes<\/strong>) and sometimes cytokines<\/strong> which stimulates the activity of macrophages<\/strong> and mast cells<\/strong>.\u00a0 Macrophages phagocytose debris and infecting pathogens (if present) as well as release chemokines to induce the chemotaxis and recruitment of other WBCs.\u00a0 Mast cells degranulate to release pro-inflammatory cytokines (e.g. histamine, bradykinin, and prostaglandins).\u00a0 Cells that are damaged are not functional, so loss of function of this tissue will occur until healing (if possible) occurs<\/li>\n
          2. The pro-inflammatory cytokines<\/strong> bind to receptors on blood vessel walls and induce vasoconstriction as well as increased capillary permeability.\u00a0 These cytokines can also trigger nociceptors resulting in pain<\/strong> sensations.\u00a0 Leaked blood can also stimulate nociceptors.\u00a0 Activated WBCs and some infectious agents release pyrogens<\/strong> as well which may give rise to fever.<\/li>\n
          3. The resulting increase in blood flow makes the tissue warm<\/strong> and red.<\/strong>\u00a0 The increase in plasma fluid entering the tissue bed results in swelling<\/strong> and pain.\u00a0 The leaked plasma fluid contains platelets and plasma proteins that assist with the immune response (e.g. fibrinogen, complement proteins, C-reactive proteins).\u00a0 Fibrin mesh and clots help to contain the area and phagocytes remove cellular debris and any pathogens.\u00a0 There is pain or swelling in a joint, muscle or bone, it may impede movement until healing occurs.<\/li>\n
          4. The WBCs that often migrate to the area include neutrophils, eosinophils, macrophages, dendritic cells, and NK cells (Natural Killer lymphocytes.\u00a0 WBCs remove infectious agents, toxins, and debris.<\/li>\n
          5. At the same time platelets and tissues release growth factors to stimulate mitosis of replacement tissue cells.\u00a0 Fibroblasts are abundant in the connective tissue throughout the body and produce collagen to help bind tissue together.\u00a0 At this point in time, when healing has begun there are three possible outcomes.<\/li>\n<\/ol>\n

            Healing<\/strong><\/h3>\n
              \n
            1. Resolution:\u00a0<\/strong> It may be that the damaged cells do not die, and recover.\u00a0 In this case, the term resolution is used and leads to return to full function.<\/li>\n
            2. Regeneration:<\/strong>\u00a0 If the tissue is small and involves cell types that are readily able to regenerate, tissue stem cells will produce daughter cells through mitosis that lead to a replacement of lost tissue with the exact same types of cells.\u00a0 This is termed regeneration.\u00a0 Many types of epithelial cells, connective tissue cells, and even liver cells are very regenerative.<\/li>\n
            3. Replacement:\u00a0 <\/strong>Cardiac muscle cells, skeletal muscle cells, kidney cells, brain and spinal cord neurons and some areas of cartilage are not very regenerative.\u00a0 In the case where damage has occured to cell types that are not regenerative or if the wound or damage is signicant, it may be that an abundance of collagen and other cell types (e.g. fibroblasts) is required to replace the lost tissue forming what is known as scar tissue.\u00a0 This process is termed fibrosis<\/strong> and involves the permanent loss of functional tissue.<\/li>\n<\/ol>\n

              During the healing process, capillaries become less permeable, and blood vessel diameter returns to normal.\u00a0 WBCs become inactivated and fibrin mesh and clots are enzymatically cleaved, dissolved and removed.\u00a0 The excess fluid in the interstitial space is absorbed by lymph vessels and returned to the bloodstream.\u00a0 The signs of inflammation (redness, warmth, swelling and pain) all diminish.<\/p>\n

               <\/p>\n

              Possible Complications of Tissue Damage and Inflammation<\/strong><\/h3>\n

              Possible complications of tissue damage and inflammation include the following:<\/p>\n

                \n
              1. Chronic Inflammation:\u00a0<\/strong> If the cause of damage is not removed (e.g. many auto-immune diseases), the perpetual damage may lead to more and more damage and activated WBCs which can cause collateral damage, delay healing and lead to fibrosis (permanent scarring and loss of functional tissue).<\/li>\n
              2. Infection:\u00a0<\/strong> If the wound is exposed to the external environment, microorganisms (even members of one’s normal flora) can become opportunistic and cause infection and therefore more damage.<\/li>\n
              3. Deep ulcers:<\/strong>\u00a0 Damage to gastric mucosa can allow for gastric acids to erode underlying tissue and damage blood vessel resulting in severe and prolonged inflammation, bleeding, necrosis, infection, possible loss of functional tissue, and fibrosis.<\/li>\n
              4. Skeletal Muscle Spasms:<\/strong> can occur as a protective response to pain during sprains (damage to ligaments) and strains (damage to muscle or tendon).\u00a0 Spasms that occur in bone fractures can force movement of broken bone ends resulting in shearing of tissue.\u00a0 (Note:\u00a0 Temporary muscle spasms (e.g. charley horse) during excessive exercise are different in that the cause is thought to be not enough blood flow, cellular dehydration, and\/or electrolyte depletion).<\/li>\n
              5. Peripheral Nerve damage:<\/strong> can lead to permanent or temorary loss of sensation, paresthesias if damage is to sensory nerves and muscle weakness or paralysis if motor neurons are affected.\u00a0 If peripheral nerve cells recover, function may be regained.\u00a0 Loss of brain or spinal cord nerves is permanent and can lead to permanent losses of function – though some brain plasiticty may occur through rehabilitation.<\/li>\n
              6. Obstruction:<\/strong>\u00a0 Swelling in the esophagus can lead to problems swallowing.\u00a0 Swelling affecting the bronchioles, bronchi, or other parts of the respiratory tract can lead to problems breathing and potentially can affect gas exchange abilities of the lungs.<\/li>\n
              7. Increased I<\/span>ntrac<\/span>ranial P<\/span>ressure (ICP):<\/strong>\u00a0 Swelling in the brain or cranial meninges can lead to increased intracranial pressures which can be fatal due to the pinching off of capillaries and reduced blood flow.<\/li>\n
              8. Myositis Ossificans:<\/strong>\u00a0 This refers to the calcification that can occassionally occur within injured muscles, most commonly the arm or thigh muscles (e.g. quadriceps).\u00a0 Risk factors include deep contusions that occur with contact sports (e.g. American football).\u00a0 The pathogenesis of calcification is unclear, but is likely linked to large reserve of available calcium in skeletal muscles tissues, as well as inappropriate differentiation of local stem cells into osteoblasts.\u00a0 Prevention may be assisted by treating deep contusions promptly with RICE (Rest, Ice, Compression, and Elevation).<\/li>\n<\/ol>\n

                 <\/p>\n

                Chronic Inflammation<\/strong><\/h3>\n

                Chronic inflammation can follow an acute episode of inflammation if the source of irritation is not entirely removed.\u00a0 It may be that the tissue continues to exposed to damage from any of the following:\u00a0 an infection (pathogen or pathogenic toxins), smoking, ingested or inhaled environmental pollutants, cancer, or chronic diseases such as diabetes, auto-immune diseases (e.g. Rheumatoid Arthritis, Systemic Lupus Erythematosus), and chronic diseases of the lungs, heart, kidneys, liver, digestive system, etc..<\/p>\n

                Chronic inflammation defers from acute inflammation in that there is:<\/p>\n

                  \n
                1. Less swelling and exudate<\/li>\n
                2. More angiogenesis<\/li>\n
                3. More lymphocytes, macrophages, & fibroblasts are present<\/li>\n
                4. Continued tissue destruction<\/li>\n
                5. More collagen produced \u2192 fibrous scar tissue (fibrosis)<\/li>\n
                6. Possible formations of Granulomas (=small mass of cells with a necrotic center, covered by connective tissue) which are long lasting.\u00a0 Granulomas may develop in rheumatoid arthritis and osteoarthritis, or\u00a0 around a foreign object (possibly involving an abscess), or at a site of chronic infection such as tuberculosis.<\/li>\n<\/ol>\n","protected":false},"author":1370,"menu_order":7,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"Pictures coming soon!","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-998","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":25,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/998","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":16,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/998\/revisions"}],"predecessor-version":[{"id":1054,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/998\/revisions\/1054"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/25"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/998\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=998"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=998"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=998"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=998"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}