28 (33). Морфофункциональная характеристика грануляционных тканей.
Грануляционная ткань или грануляции (от лат. granum — зерно) — молодая соединительная ткань, образующаяся при процессах заживления дефектов в различных тканях и органах. Развитие грануляций — приспособительный процесс, который содействует заживлению ран и язв, организации и элиминации инородных тел и нежизнеспособных тканей.
Вследствие повреждения ткани развивается травматический отёк, избыточное накопление жидкости, в которой содержится большое количество белков. Сменяющая отёк воспалительная реакция расплавляет мертвые ткани и очищает рану, а по мере ее завершения начинают развиваться грануляции, постепенно заполняющие возникший дефект.
Грануляционная ткань имеет различный вид в зависимости от стадии её развития. Нормальная ткань изначально имеет вид нежнозернистой ткани, покрытой мутноватым, серо-зеленоватым налетом, сочна, богата тонкостенными сосудами, из-за чего легко кровоточит. В более поздних периодах ткань становится бледнее, плотнее, зернистость исчезает, превращаясь в беловатый плотный рубец.
Грануляционная ткань состоит из шести, постепенно переходящих друг в друга слоев:
— поверхностный лейкоцитарно-некротический слой;
— поверхностный слой сосудистых петель;
— слой вертикальных сосудов;
— слой горизонтально расположенных фибробластов;
В случаях благоприятного течения раневого процесса по мере очищения раны от мертвой ткани на 3-5 сутки раневой процесс постепенно переходит в стадию гранулирования. У лошадей появление грануляций наблюдается в участках гнойно-ферментативного очищения раны от мертвых тканей, а у КРС и свиней – непосредственно под струпом в границах здоровой ткани. Формирование грануляционной ткани происходит по мере очищения раны от мертвых тканей и снижения воспалительной реакции. В участках полного отторжения мертвых тканей раневая поверхность покрывается раневым секретом, представляющим собой мутноватую жидкость тягучей консистенции соломенного цвета, в котором содержатся некрогормоны, трефоны, проеоглюкины, гликопротеиды и другие физиологически активные и питательные вещества.
В раневом секрете в относительно небольшом количестве ткаже содержатся вазогенные клетки и фибробласты. В последующем раневой секрет подсыхает, превращается в корочки, под которыми и протекает процесс гранулирования. Раневой секрет = среда, которая стимулирует грануляционный процесс (образование первичных сосудистых дуг, пролиферация клеточных элементов и фибробластический процесс). Слабокислая реакция раневой среды, отрицательный электропотенциал раневого секрета и стимулирующее влияние трефонов, некрогормонов и медиаторов воспаления способствует возникновению капилляров.
Сформировавшаяся сеть капилляров вначале имеет беспорядочное расположение в грануляциях, но в последующем принимает вид правильно расположенных сосудов, дифференцирующихся в структурно-функциональном отношении. Сосуды, идущие к поверхности раны, приобретают функцию артериощ, а направляющиеся от гранулирующей поверхности вглубь – вен. За 4-5 дней раневая поверхность оказывается покрытой сплошной грануляционной тканью.
По мере роста грануляции в глубоких слоях происходит рубцевание, а в средних – созревание грануляционной ткани с превращением ее в зрелую соединительную. Формирующаяся в глубине грануляционного пласта рубцовая ткань стягивает края раны к ее центру.
В процессе воспаления формируется грануляционная ткань, отграничивающая повреждение и участвующая в заживлении ран.
Грануляционная ткань – это своеобразный «временный орган», создаваемый организмом в условиях патологии для реализации защитной и репаративной функции соединительной ткани.
Грануляционная ткань (лат. granulum зернышко; синоним зернистая ткань) — соединительная ткань, образующаяся при заживлении ран, организации инфарктов, тромбов, экссудатов, инкапсуляции инородных тел.
Этапы формирования грануляционной ткани:
• Протеолитическое разрушение базальной мембраны сосудов и миграция клеток крови.
• Миграция эндотелиальных клеток в направлении ангиогенного стимула.
• Пролиферация эндотелиальных клеток.
• Созревание эндотелиальных клеток и их организация в капилляры.
Состав грануляционной ткани – клетки крови, эндотелиальные клетки,капилляры,фибробласты.
Весь цикл развития и созревания Г. т. занимает в среднем 2—3 нед. Однако различные этапы этого процесса могут затягиваться или протекать интенсивнее в зависимости от размеров раны, индивидуальных особенностей организма, различных условий окружающей среды и методов лечения. В случае отклонения от описанного хода развития Г. т. (например, при нарушениях иннервации, кровообращения, авитаминозе и др.) наблюдаются вяло текущие грануляции или их чрезмерно быстрое созревание с формированием избыточных грубых рубцов, называемых келоидными.
Неповрежденная грануляционная ткань является стойким защитным раневым барьером, препятствующим всасыванию в организм ядовитых продуктов тканевого распада, микробов и продуктов их жизнедеятельности. Грануляционная ткань связывает, разжижает и обезвреживает токсины и ядовитые продукты тканевого распада, подавляет жизнедеятельность микробов, продуцирует антитела. Микробы, находящиеся в гнойном экссудате, на поверхности грануляций или проникшие в грануляционную ткань, погибают или значительно теряют свою вирулентность.
Granulation Tissue
Granulation tissue is an important component of the pathophysiology of CSOM.
Related terms:
Skin Flap Physiology and Wound Healing
Paul W. Flint MD, FACS , in Cummings Otolaryngology: Head and Neck Surgery , 2021
Formation of Granulation Tissue
At approximately 3 to 4 days following injury, a new stromal framework—known as granulation tissue —begins to enter the wound and replace the fibrin clot. Granulation tissue consists of a dermal matrix that provides a framework for cell migration, which is enhanced by angiogenesis.
The cell that is most important in the production of the dermal matrix is the fibroblast. 303 Fibroblasts enter the wound by 2 to 3 days, and within the first week, they become the dominant cell population in the wound. PDGF and EGF, produced by platelets and macrophages, are the main signals to the fibroblasts. 280 As fibroblasts migrate into the wound, they become activated, begin synthesizing collagen, and proliferate. 287 The initial wound matrix is primarily composed of fibrin and fibronectin. Fibrin is gradually replaced by collagen and other proteins such as glycoproteins, which are a key component of the mature matrix and are actively synthesized during this part of healing. Aberrations in collagen result in abnormal wound healing. Impaired activation of inflammatory cells in disorders such as diabetes, results in limited collagen deposition and impaired wound healing. Conversely, keloid formation is a result of excess collagen formation. 304 Collagen imparts integrity and strength to tissues and plays an important role in the proliferative and remodeling phases.
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The fibroblast is critical to the production of the dermal matrix and produces type I and III collagens, fibronectin, elastin, and proteoglycans. After the first week, abundant ECM further supports cell migration.
Angiogenesis
The newly formed granulation tissue requires a vascular supply to provide for its metabolic needs. The process of angiogenesis begins at the time of injury. Cell disruption and hypoxia, hallmarks of tissue injury, are strong inducers of angiogenesis factors. Acidic fibroblast growth factor (FGF)-1 and FGF-2 are released from disrupted cells and have potent angiogenic activity. 305,306 Hypoxia stimulates macrophages and keratinocytes to produce the angiogenic vascular endothelial growth factor (VEGF). 292,307 VEGF and TNF-α result in the formation of new endothelial cells and capillaries at the wound edges. 297,308 NO also stimulates VEGF production and appears to contribute to granulation tissue formation by triggering endothelial migration, proliferation, and differentiation; thus it participates in capillary ingrowth into the wound site during repair. 309,310 Increased VEGF production also encourages vasodilation and angiogenesis. Other growth factors known to enhance angiogenesis are PDGF, heparin binding EGF, IGF-1, and hepatocyte growth factor. 305
Fibrotic Response to Biomaterials and all Associated Sequence of Fibrosis
Granulation tissue and the foreign body reaction
Granulation tissue is vascularized tissue that forms as chronic inflammation evolves. The new capillaries make the tissue appear pink and granular, thus the name. Histologically, one can observe macrophages and proliferating fibroblasts within granulation tissue. This tissue can appear as early as 3–5 days after biomaterial implantation. In the early stages of granulation tissue production, proliferating fibroblasts produce primarily proteoglycans, while later they produce mostly type III collagen ( Utsunomiya et al., 2005 ). In the presence of a persistent stimulus, granulation tissue, or chronic inflammation, can endure for the duration of the presence of the biomaterial. In some cases, wear debris or corrosion products are released throughout the lifetime of the implant. Hip implants are well known for producing such debris and causing concomitant damage (see Chapter 12 ). Degradable biomaterials have the potential to elicit such a response as well, depending on the mode of degradation ( Galgut et al., 1991 ). In other cases, there is continuing injury due to biomaterial movement or mismatch of mechanical properties with the native tissue which serve as stimuli for granulation tissue formation.
In addition to granulation tissue, nondegradable and slowly degradable biomaterials generally elicit a foreign body response. This response has been described in Chapter 2 .
Benign Vocal Fold Mucosal Disorders
Paul W. Flint MD, FACS , in Cummings Otolaryngology: Head and Neck Surgery , 2021
Polypoid Granulation Tissue
Fechner and colleagues 92 reviewed 639 vascular lesions of the head and neck, 62 of which were found in the larynx or trachea, and reported that polypoid granulation tissue is the most common vascular tumor in the larynx. They also noted that pyogenic granuloma does not occur in the larynx. Pyogenic granuloma, as seen most often on the tongue, consists of distinct lobules of capillaries separated by fibromyxoid stroma, whereas polypoid granulation tissue consists of radially arranged capillaries. These investigators attribute formation of polypoid granulation tissue in the larynx to one of several forms of trauma (i.e., caused by laryngeal biopsy, intubation, direct external trauma to the larynx, and an external penetrating wound). Granulation tissue in the larynx should be handled primarily by conservative measures that include removal of the source of any ongoing irritation, such as from inappropriate voice use or from acid reflux laryngitis, and intralesional corticosteroids. For nonresponse and continuing symptoms, careful endoscopic removal may be considered after the granulation tissue has been allowed to mature and to become less active and vascular.
Office Management of Tympanic Membrane Perforation and the Draining Ear
Peter S. Roland , . Joe W. Kutz , in Otologic Surgery (Third Edition) , 2010
Pathophysiology
Granulation tissue is almost an invariant accompaniment of CSOM. It can develop quickly in a draining ear, and is already present in many infections of less than 6 weeks’ duration. The presence of granulation tissue, especially when it is abundant, may be a factor that contributes to treatment failure of acute infections, and the evolution of AOM into CSOM. The formation of granulation tissue in the middle ear begins with a break in the basement membrane of the surface epithelial cells. Inflammatory cells in the underlying lamina propria traverse through the broken basement membrane and enter the lumen of the middle ear space. The rupture of the basement membrane and epithelial lining cell is caused by bacterial toxins, inflammatory mediators produced by ruptured liposomes, and the accumulation of subepithelial fluid and vacuoles, all of which exert pressure on the surface epithelium. 14
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The next step in the formulation of granulation tissue occurs when a small piece of the herniated lamina propria extrudes through the ruptured area between epithelial cells. Initially, the extruded lamina propria pushes into the middle ear without any epithelial covering. Angiogenic growth factors incite capillary budding, vascular hyperpermeability, and fibroblast recruitment—that is, granulation tissues form. If the growth of granulation tissue is vigorous and aggressive, polyps develop. 15 Meyerhoff and colleagues 10 evaluated temporal bone from subjects with CSOM and reported that granulation tissue develops in 90% of all CSOM, and in 100% of cases of CSOM that develop intracranial complications.
Wound healing
Geoffrey C. Gurtner MD, FACS , in Plastic Surgery: Volume 1: Principles , 2018
Granulation tissue
The fibrin clot formed during hemostasis participates in the early inflammatory phase and is replaced by a perfused, fibrous connective tissue that grows from the base of a wound and is able to fill wounds of almost any size. During the proliferative phase of wound healing, this granulation tissue is light red or dark pink in color because of perfusion by new capillary loops. It is soft to the touch, moist, and granular in appearance. The granulation tissue serves as a bed for tissue repair. The ECM of granulation tissue is created and modified by fibroblasts. Initially, it consists of a network of type III collagen, a weaker form of the structural protein that can be produced rapidly. This is later replaced by the stronger, long-stranded type I collagen, as evidenced in scar tissue. Formation and contraction of the granulation tissue represent integral aspects of the healing wound. In ischemic wounds, production and contraction of the granulation tissue is impaired because of decreased ATP production, impaired collagen synthesis and failure to convert the fibroblast phenotype into a myofibroblast to promote wound contraction. 65
Benign Conditions of the Vagina
Granulation Tissue
Granulation tissue is a common cause of postsurgical vaginal bleeding and frequently is biopsied, particularly if there are concerns stemming from a prior surgical procedure for a neoplasm. Typically, granulation tissue appears as a raised red, lobular lesion in the upper vagina, near or within the sutured cuff. The histologic features are characteristic, with abundant vascular growth, epithelial erosion, and intense inflammation ( Fig. 11.9 ). The process evolves (heals) over time, with a greater proportion of the lesion being occupied by fibrous tissue with less prominent vessels.
In some cases, abundant squamous cells can be trapped within the granulation tissue, giving the false impression of a squamous neoplasm. However, at higher power, the two components can be distinguished ( Fig. 11.10 ).
Inflammatory Disorders of the Esophagus
REACTIVE CHANGES IN ULCERS VERSUS DYSPLASIA/CARCINOMA
Granulation tissue within the base of erosions or ulcers may exhibit large atypical endothelial cells and fibroblasts 37 , 38 ( Fig. 11-7 ). They are usually distributed in a scattered fashion within otherwise typical granulation tissue. Furthermore, these cells do not form solid clusters of cells and have a normal, or even decreased, nucleus-to-cytoplasm (N/C) ratio. In contrast, carcinoma usually demonstrates groups or sheets of cohesive cells with overlapping nuclei and an increased N/C ratio. In difficult cases, immunohistochemistry for cytokeratins can be helpful in differentiating true carcinoma (positive) from reactive “pseudosarcomatous” alterations of the stromal cells (negative).
Rarely, the inflammatory exudate within the ulcer or erosion may contain abundant activated and atypical lymphocytes that can simulate lymphoma ( Fig. 11-8 ). In general, these cells are typically benign when confined to the surface exudate. The infiltrate should raise concern for a lymphoma when it involves the underlying tissue in a dense confluent and homogeneous manner.
Surgery in Nonhuman Primates
Overgrown Granulation Tissue
Granulation tissue formation is part of a normal healing process. Under certain conditions, such as infection, self-mutilation, or a local reaction to a chronically implanted, foreign material, this tissue grows uncontrollably and becomes very vascular and secretive. Treating local infections, frequent cleaning of the interfaces and removal of cellular debris, removal of foreign bodies, cauterizing or trimming under local block, or anesthesia may facilitate management of granulation tissue. Use of topical corticosteroids is of limited value. Other agents such as anti-mitotic 5-flurouracil (5-FU) have been used to control the growth of tough supradural connective tissue inside the chronic cranial recording chambers. 5-FU has been shown to minimize the dural growth and scar tissue formation by depressing the fibroblast division, to reduce vascularization and blood loss during removal, to reduce the number of necessary procedures to remove the growing tissue, and inhibit bacterial infections over a period of 15–30 weeks ( Spinks et al., 2003 ). Sometimes the therapeutic efforts fail and force an explantation surgery, a radical but effective resolution.
Wound healing
Christopher L.B. Lavelle PhD, DSc, DDS, MRCPath, FRCD , in Applied Oral Physiology (Second Edition) , 1988
Granulation tissue
Granulation tissue comprises a dense population of macrophages, fibroblasts and newly forming blood vessels in a loose matrix of collagen, fibronectin and hyaluronic acid. Re-epithelialization of an oral epithelial wound begins within the first 24 h after injury, i.e. several days prior to granulation tissue formation, although in fact both are intimately associated with one another.
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Re-epithelialization of a mucosal wound begins within hours of injury by epithelial cell movement from the free edge of the tissue across the defect. 37 Such epithelial cell movement occurs following the metamorphosis associated with loss of apical–basal polarity and extension of pseudopodia from the free basolateral side into the wound. Such epithelial cell migration does not depend on mitosis 38 but is probably associated with chemotactic factors and active contact guidance, although other factors may also be involved. Within a short period of time the epithelial cells remaining at the edge of the wound begin to proliferate in order to generate an additional population of migrating cells, 39 although whether this is associated with chalones or other local growth factors remains obscure. During re-epithelialization of a wound in which the basement membrane has been disrupted, the basement membrane does not reform until after epithelial migration ceases. 40 As the epithelial cells cease to migrate, type IV collagen and then laminin 41 are produced, beginning at the wound margin, progressing inwards, simulating a zipper mechanism that interlocks the new epithelial and new connective tissue structures. Subsequently, the epithelial cells become firmly attached to the basement membrane by hemidesmosomal formation.
Although the chemical mediators remain obscure, the local proliferation and invasion of fibroblasts into the wound is crucial for healing. Such invasion is predicated on the prior metamorphosis of the fibroblasts to myofibroblasts, where the cells gain motile and contractile properties in addition to their secretory and synthetic capacities. As these myofibroblasts migrate into the wound defect, they concomitantly deposit a loose extracellular matrix comprising predominantly fibronectin. 42 This fibronectin matrix not only appears to be associated with fibroblastic adhesion and growth but is also associated with initial wound contraction and orientation of subsequently produced collagen fibrils.
The invasion of newly formed blood vessels into the site of a wound occurs simultaneously with fibroblastic proliferation, conceivably under the direction of chemical mediators derived from the oral epithelium and underlying connective tissue, in addition to low oxygen tension, 43 lactic acid 44 and biogenic enzymes. Furthermore, whether this vascular invasion centres on mitogenic or migratory cellular activity remains obscure.
The third and final stage of wound healing centres on matrix formation and remodelling. In fact, matrix formation begins at the time of granulation tissue formation, although the matrix is then constantly altered to accommodate functional demands. Such changes involve fibronectin replacement with large fibrous bundles of type I collagen that provide the residual scar with increasing tensile strength.
The initial deposits of extracellular matrix contain predominantly fibronectin, which may serve as a template for collagen deposition. 46 In fact, the fibronectin matrix is replaced by type III and then type I collagen. 47 Although collagen provides a less adherent surface for fibroblasts compared with fibronectin, 48 these types of collagen ultimately form fibrous bundles that greatly enhance the tensile strength.
Hyaluronic acid is another component of granulation tissue that is critical in early fibroblastic proliferation. As granulation tissue matures, however, hyaluronic acid is decreased by tissue hyaluronidase 49 and replaced by proteoglycans. 50 This latter is not so conducive to cell migration but serves to increase tensile strength and resilience. The enormous molecular versatility permits proteoglycans to have many diverse structural and functional tissue activities. These substances promote fibrogenesis by fibroblasts 51 and mediate cellular adhesion and influence the budding of new blood vessels.
At least three classes of collagens occur in connective tissue: fibrillar collagens (types I, II and III); basement membrane collagen (type IV) and pericellular collagens (type V). In addition to providing tensile wound strength, these collagens influence cell activity.
Local Wound Care for Palliative and Malignant Wounds
Kevin Y. Woo , R. Gary Sibbald , in Palliative Care (Second Edition) , 2011
H: Hemorrhage or Bleeding
The granulation tissue within a malignant wound bleeds easily due to local stimulation of vascular endothelial growth factor (VEG-F), resulting in excess formation of abundant but fragile blood vessels. Reduced fibroblast activity and ongoing thrombosis of larger vessels in infected and malignant wounds may compromise the strength of collagen matrix formation, rendering the granulation less resilient to trauma. 30 Even minor trauma from the removal of wound dressings that adhere to wound surface can provoke bleeding. 31 Other health conditions (e.g., abnormal platelet function, vitamin K deficiency) may also put patients with cancer and other terminal diseases at risk of bleeding. Frank hemorrhage can occur as the tumor erodes into a major blood vessel.
A variety of hemostatic agents can be applied topically to control hemorrhage ( Table 17-2 ). In severe cases, suturing a proximal vessel, intravascular embolization, laser treatment, cryotherapy, radiotherapy, or electrical cauterization may be necessary. 32
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