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Granulation tissue

Granulation tissue is a type of new connective tissue rich in microscopic blood vessels and inflammatory cells that forms on the surfaces of wounds, ulcers, or inflamed tissues during the healing process, particularly in wounds healing by secondary intention.^[1] It appears as pink or red, soft, moist, and bumpy tissue that fills the wound bed, providing a scaffold for epithelial cell migration and tissue regeneration.^[1] The formation of granulation tissue occurs during the proliferative phase of wound healing, typically days to weeks after injury, when fibroblasts, endothelial cells, keratinocytes, and myofibroblasts proliferate to replace the initial fibrin clot with a provisional extracellular matrix composed primarily of type III collagen, proteoglycans, hyaluronic acid, and elastin.^[1] Histologically, it is characterized by an abundance of new capillaries, plump fibroblasts, reactive endothelial cells, and a mixed inflammatory infiltrate, which collectively support revascularization, protect against infection, and enable wound contraction through the action of myofibroblasts.^[1] Over time, this tissue matures, with type III collagen being remodeled into stronger type I collagen, eventually leading to scar formation as the wound closes.^[1] Clinically, healthy granulation tissue is essential for proper wound closure but can become problematic if excessive or persistent, often signaling underlying issues such as infection, foreign bodies, ischemia, or chronic conditions like diabetes and vascular insufficiency, in which case it may appear dark red, friable, and prone to bleeding, necessitating interventions like debridement or antimicrobial therapy.^[1]

Overview and Characteristics

Definition

Granulation tissue is a temporary connective tissue matrix rich in new capillaries, fibroblasts, and inflammatory cells that forms to fill wound defects during the proliferative phase of wound healing.^[1] This matrix arises primarily in wounds healing by secondary intention, where significant tissue loss occurs, and serves as a foundational scaffold for subsequent tissue repair.^[1] Unlike the initial fibrin clot that stabilizes the wound in the early inflammatory stage, granulation tissue represents a more organized proliferative response, eventually giving way to mature scar tissue characterized by dense, collagen-rich acellular bands during the remodeling phase.^[2]^[3] The tissue derives its name from the Latin granum, meaning "grain," alluding to its bumpy, granular texture formed by protruding loops of newly formed capillaries.^[4] This pink-to-red appearance stems from the abundance of these capillary loops and associated inflammatory infiltrate, creating a soft, moist surface that facilitates epithelial migration.^[5] The term "granulation tissue" entered medical literature in the late 19th century, with its first documented use around 1873, reflecting observations in pathology texts of healing wounds and ulcers.^[6] Granulation tissue can form in wounds of varying depths and locations, often manifesting as exuberant proliferations in specific contexts. For instance, pyogenic granuloma represents an example of localized vascular proliferation resembling granulation tissue, typically arising from minor trauma or irritation on skin or mucosal surfaces.^[7] Similarly, in dental pathology, pulp polyps—also known as chronic hyperplastic pulpitis—exhibit granulation tissue growth protruding from exposed pulp chambers in carious teeth.^[8] These examples highlight the tissue's adaptive role in filling defects across different tissue types.

Appearance

Granulation tissue exhibits a distinctive macroscopic appearance that facilitates its identification in clinical practice. Healthy granulation tissue typically presents as a soft, moist, and bumpy surface with a granular or cobblestone texture, resembling grains of sand or "proud flesh," and its color ranges from light pink or red in early stages to a brighter, beefy red or dark pink in mature phases due to the perfusion of new capillary loops.^[1]^[9]^[10]^[11] The tissue is generally painless, though it is friable and bleeds easily upon contact due to fragile new vessels. In contrast to pale, dry eschar or yellow, sloughy debris in stalled wounds, healthy granulation appears shiny and moist, signaling active repair, while unhealthy variants may show darker red hues, excessive friability, or a painful quality indicative of infection or poor perfusion.^[1]^[9]^[10] Excessive growth, known as hypergranulation or proud flesh, manifests as raised, mushroom-like tissue protruding beyond the wound edges, often with a red, friable, and shiny surface that can delay healing if unmanaged.^[12]^[13] Clinically, granulation tissue is assessed through direct visual inspection or endoscopy, where its presence and uniform, advancing growth confirm progressing wound healing, prompting gentle handling to preserve the delicate structure.^[1]^[11]

Histological Features

Under light microscopy, granulation tissue appears as a loose, edematous stroma populated by proliferating fibroblasts, endothelial cells forming new capillary loops, and scattered inflammatory cells such as macrophages and neutrophils.^[1] This matrix is richly vascularized, with the tissue typically staining pink on hematoxylin and eosin (H&E) preparations due to the presence of immature collagen and abundant small blood vessels.^[1] The overall architecture is disorganized, serving as a provisional scaffold during the proliferative phase of wound healing.^[14] Key histological identifiers include parallel arrays of capillary loops oriented perpendicular to the wound surface, which facilitate nutrient delivery and contribute to the tissue's characteristic vascularity.^[1] Early granulation tissue also features nascent myofibroblasts, differentiated from fibroblasts and expressing α-smooth muscle actin, which enable wound contraction through interactions with the extracellular matrix.^[14] Organized epithelium is absent in pure granulation tissue until the re-epithelialization phase, when keratinocytes migrate across the surface.^[1] In diagnostic biopsies, granulation tissue exhibits a disorganized, loosely arranged matrix, distinguishing it from keloids, which show dense, nodular bundles of thick, hyalinized collagen fibers.^[15] Electron microscopy further reveals immature collagen fibrils with initial diameters of approximately 10-20 nm, reflecting the early synthetic stage before maturation into larger, organized fibers.^[16]

Formation and Development

Phases of Wound Healing

Wound healing proceeds through four overlapping phases: hemostasis, inflammation, proliferation, and remodeling. The hemostasis phase occurs immediately after injury, lasting from zero to several hours, during which vasoconstriction and platelet aggregation form a fibrin clot to stop bleeding and provide a provisional matrix.^[17] This is followed by the inflammation phase, typically spanning days 1 to 3, where neutrophils and macrophages infiltrate the site to clear debris, bacteria, and damaged tissue through phagocytosis and release of cytokines.^[18] The proliferation phase, from approximately days 4 to 21, involves the synthesis of new tissue, including epithelialization, angiogenesis, and collagen deposition to fill the wound defect.^[19] Finally, the remodeling phase begins around week 3 and can extend for weeks to years, characterized by collagen reorganization, wound contraction, and increased tensile strength, ultimately forming a mature scar with about 80% of original tissue strength.^[17] Granulation tissue emerges during the transition from the late inflammatory to the early proliferative phase, typically starting 1 to 2 days post-injury as fibroblasts begin migrating into the clot.^[20] It peaks in formation around 5 to 7 days after injury, when vascular proliferation and extracellular matrix deposition are most active, creating a pink, granular bed that supports reepithelialization.^[20] The duration of granulation tissue development varies by wound type; in acute wounds, it resolves within 2 to 3 weeks as the tissue matures, whereas in chronic wounds, it may persist indefinitely due to stalled progression.^[17] Several factors influence the timing of these phases, particularly the onset and progression of granulation tissue formation. Larger wound size can prolong the inflammatory phase and delay proliferation by increasing the volume of debris to clear.^[19] Infection exacerbates inflammation, extending its duration and impeding the shift to proliferation.^[18] Inadequate oxygenation, often due to poor perfusion, hinders fibroblast activity and angiogenesis essential for granulation.^[17] For instance, diabetic ulcers frequently delay the proliferative phase because of hyperglycemia-induced neuropathy, ischemia, and impaired immune responses, leading to prolonged inflammation and reduced granulation tissue formation.^[20] Molecular signals, such as growth factors released by macrophages, trigger the proliferative phase but are detailed in cellular mechanisms.^[19]

Cellular and Molecular Mechanisms

The formation of granulation tissue is driven by intricate cellular and molecular processes that coordinate cell migration, proliferation, and matrix remodeling following injury. Fibroblasts play a central role, migrating and proliferating in response to platelet-derived growth factor (PDGF) and transforming growth factor-β (TGF-β), which are released primarily from platelets, endothelial cells, and macrophages to stimulate fibroblast activation and collagen synthesis.^[21] Endothelial cells are activated for angiogenesis through vascular endothelial growth factor (VEGF), promoting their proliferation and migration to form new capillaries essential for tissue oxygenation and nutrient delivery.^[21] Inflammatory cell recruitment is mediated by chemokines such as interleukin-8 (IL-8), which attracts neutrophils and other leukocytes to the wound site, facilitating debris clearance and amplification of the repair response. Early in the process, tissue hypoxia upregulates hypoxia-inducible factor-1α (HIF-1α), which in turn induces VEGF expression to initiate angiogenesis.^[21] Concurrently, matrix metalloproteinases (MMPs), secreted by fibroblasts and macrophages, degrade the provisional fibrin matrix, enabling cellular invasion and deposition of a new extracellular scaffold.^[21] Growth factors like fibroblast growth factor (FGF), derived from platelets and macrophages, further support mitogenesis and vascularization during granulation tissue expansion.^[21] Negative regulators, such as thrombospondin-1, counteract excessive angiogenesis and tissue overgrowth by inhibiting endothelial cell responses and limiting granulation tissue formation. These mechanisms ensure balanced progression from inflammation to proliferative repair.

Composition

Cellular Components

Granulation tissue is primarily composed of fibroblasts, which constitute the dominant cellular population and are essential for matrix production and tissue remodeling. These mesenchymal-derived cells migrate into the wound site during the proliferative phase of healing, where they synthesize provisional extracellular components to support tissue reconstruction. Under the influence of transforming growth factor-beta (TGF-β), fibroblasts differentiate into myofibroblasts, characterized by the expression of alpha-smooth muscle actin (α-SMA), enabling wound contraction and enhanced mechanical force generation.^[22]^[23] Inflammatory cells play a critical role in the early stages of granulation tissue formation by clearing debris and orchestrating repair. Neutrophils predominate in the initial 1-2 days post-injury, providing antibacterial defense through phagocytosis and release of reactive oxygen species to combat infection. Macrophages peak around day 3 in mouse models or up to day 7 in humans, performing phagocytosis of apoptotic neutrophils and pathogens while secreting cytokines such as TGF-β to recruit fibroblasts and promote tissue repair. Lymphocytes, including T cells, contribute to adaptive immunity and resolution of inflammation, becoming more prominent in later phases to modulate the healing environment.^[1]^[22] Other cell types support the structural and functional integrity of granulation tissue. Endothelial cells drive capillary formation by proliferating and migrating in response to vascular endothelial growth factor (VEGF), establishing a vascular network essential for nutrient delivery. Mast cells release histamine to increase vascular permeability, facilitating immune cell infiltration during the inflammatory transition. Mesenchymal stem cells, recruited from bone marrow, contribute to granulation tissue by differentiating into fibroblasts and secreting growth factors that enhance overall repair processes.^[1]^[22]^[24]

Extracellular Matrix

The extracellular matrix (ECM) of granulation tissue serves as a provisional scaffold that supports cellular migration and tissue reorganization during the proliferative phase of wound healing. This matrix is primarily composed of fibronectin, hyaluronic acid, and type III collagen, which forms fine reticular fibers providing structural flexibility. Fibronectin, a glycoprotein, facilitates cell adhesion and migration by binding to integrins on fibroblasts and endothelial cells, while hyaluronic acid, a nonsulfated glycosaminoglycan, maintains a hydrated, gel-like environment conducive to cellular infiltration.^[25]^[26] Glycosaminoglycans, including hyaluronic acid and proteoglycans, play a critical role in ECM hydration and swelling, enabling the matrix to expand and accommodate proliferating cells without excessive stiffness. These components are synthesized predominantly by fibroblasts, which upregulate procollagen mRNA in response to growth factors such as transforming growth factor-beta (TGF-β), leading to the secretion of type III collagen as the dominant fibrillar protein in early granulation tissue. Initially, type III collagen predominates, comprising approximately 50% of total collagen, with the ratio of type III to type I around 1:1, reflecting the need for a compliant matrix; this ratio reverses during the remodeling phase as type I collagen accumulates for enhanced durability.^[27]^[28] The ECM exhibits high turnover dynamics, driven by matrix metalloproteinases (MMPs) such as MMP-2 and MMP-9, which degrade provisional components to allow continuous remodeling and prevent fibrosis. This enzymatic activity ensures the matrix provides a temporary scaffold for cell migration while adapting to mechanical stresses. Consequently, granulation tissue has low tensile strength, typically ranging from 1-5 MPa, in contrast to mature scars that exceed 50 MPa due to cross-linked type I collagen fibers.^[26]^[27]

Vascular Components

Granulation tissue features a dense network of newly formed blood vessels, primarily consisting of thin-walled, tortuous capillary loops that arise through sprouting angiogenesis from preexisting vessels at the wound margins. These capillaries are lined by endothelial cells and stabilized by pericytes, which provide structural support and regulate vessel permeability and maturation. The vascular density in granulation tissue peaks at approximately 10-20% of the tissue volume, significantly higher than in normal skin, contributing to the tissue's characteristic reddish appearance due to the abundance of these immature vessels. Intussusceptive angiogenesis, involving the splitting of existing vessels, also contributes to the expansion of this network, particularly in later stages of formation.^[1]^[29] The formation of these vascular components begins during the proliferative phase of wound healing, with new vessels typically emerging by days 3-5 post-injury as granulation tissue develops. Hypoxia in the wound bed, peaking around day 4, triggers the production of vascular endothelial growth factor A (VEGF-A) by macrophages and other hypoxic cells, promoting endothelial cell proliferation, migration, and sprouting from parent vessels. Angiopoietin-1, secreted by pericytes and supporting cells, facilitates vessel maturation by enhancing endothelial-pericyte interactions and stabilizing the nascent capillaries. Following peak angiogenesis around days 4-7, excess vessels regress through apoptosis and pruning as healing progresses, restoring vascular density to levels similar to uninjured tissue. VEGF signaling pathways, detailed elsewhere, underpin these processes but are initiated here by local hypoxic cues.^[30]^[31]^[32]^[33]^[34] These vessels primarily function to deliver oxygen and nutrients to the healing site, maintaining tissue partial pressure of oxygen (PO₂) at approximately 10-25 mmHg, which supports cellular metabolism and proliferation despite the hypoxic environment. Additionally, lymphatic vessels sprout concurrently with blood vasculature, aiding in the drainage of excess interstitial fluid to control edema and prevent excessive swelling in the granulation tissue. Pericyte coverage ensures vessel integrity, minimizing leakage and facilitating efficient nutrient exchange within the provisional matrix.^[35]^[36]

Functions

Role in Tissue Repair

Granulation tissue acts as a provisional bridge in the wound healing process, filling the defect created by injury and serving as a temporary extracellular matrix that supports the migration of epithelial cells across the wound bed to achieve re-epithelialization. This matrix, rich in fibronectin, proteoglycans, and initially type III collagen, provides a structural scaffold that facilitates cell adhesion and movement, while myofibroblasts within the tissue drive wound contraction through actin-mediated forces, reducing the wound area by up to 20-30% in human cases of secondary intention healing.^[37] The alignment of this matrix during contraction further guides the oriented deposition of collagen fibers, laying the foundation for subsequent scar formation and ensuring organized tissue regeneration.^[1]^[38]^[39] As healing progresses, granulation tissue transitions to the remodeling phase, where type III collagen, predominant in the early matrix, undergoes increased cross-linking mediated by lysyl oxidase, an enzyme that oxidizes lysine residues to form stable covalent bonds and enhance tensile strength. This process strengthens the provisional matrix, preparing it for replacement by more durable type I collagen, while the vascular components of granulation tissue supply essential oxygen and nutrients to sustain repair activities. Myofibroblasts, key to contraction, subsequently undergo apoptosis after wound closure, reducing cellularity and preventing excessive fibrosis as the tissue matures into scar.^[40]^[1]^[41] The proliferative phase dominated by granulation tissue typically spans 2-4 weeks, during which wound contraction progresses at a rate of approximately 0.5-1 mm per day, with its volume directly correlating to overall healing efficiency. Adequate granulation formation promotes timely closure, but disruptions—such as impaired angiogenesis or persistent inflammation—can stall this advance, leading to failure in matrix resolution and the development of chronic ulcers.^[42]^[38]^[1]

Immune Response

Granulation tissue plays a critical role in orchestrating the immune response during wound healing, particularly through phagocytosis mediated by macrophages and neutrophils to control infections and clear debris. Neutrophils and M1-polarized macrophages engulf bacteria and dead cells, utilizing reactive oxygen species (ROS) for microbial killing and releasing pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1) to amplify the response.^[43] Macrophages exhibit plasticity, initially adopting an M1 phenotype that promotes inflammation and phagocytosis via ROS production, before transitioning to an M2 phenotype that supports repair by efferocytosing apoptotic neutrophils and secreting anti-inflammatory factors. This polarization is essential for balancing defense against pathogens and preventing excessive tissue damage in the granulation phase.^[44] Antimicrobial defense in granulation tissue is further bolstered by the production of antimicrobial peptides and activation of the complement system. Keratinocytes contribute defensins, such as human β-defensin-3, which exhibit broad-spectrum antibacterial activity and enhance immune cell recruitment to the wound bed. Complement activation, particularly through the alternative pathway involving C3 and C5, opsonizes pathogens for enhanced phagocytosis by neutrophils and macrophages while generating anaphylatoxins like C5a that promote chemotaxis and oxidative bursts.^[45] These mechanisms collectively ensure efficient clearance of microbial invaders within the extracellular matrix of granulation tissue.^[43] The resolution of the immune response in granulation tissue involves regulatory mechanisms to dampen inflammation and facilitate progression to repair. Regulatory T-cells (Tregs) infiltrate the site, releasing interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β) to suppress pro-inflammatory signals, promote M2 macrophage polarization, and prevent chronic activation. However, dysregulated excessive inflammation, often driven by elevated levels of interleukin-6 (IL-6) from macrophages and other cells, can prolong the response and delay granulation tissue maturation.^[43] Neutrophil recruitment, as detailed in cellular components, supports initial phagocytosis but must be resolved to avoid fibrosis.

Clinical Relevance

Normal Healing Process

In uncomplicated wounds, granulation tissue formation typically begins around days 3 to 5 post-injury, during the proliferative phase of wound healing, as inflammation subsides and fibroblasts, endothelial cells, and macrophages migrate into the wound bed to initiate tissue repair.^[17] By approximately week 2, the tissue matures, with increased vascularization, collagen deposition, and organization into a more structured matrix that supports reepithelialization.^[46] Regression commences around week 4, as excess vessels regress and the provisional matrix remodels into a stable scar through apoptosis and extracellular matrix reorganization.^[1] Key indicators of healthy progression include an even, beefy red granulation bed that appears moist and granular without friability, alongside advancing epithelial margins that migrate across the wound surface.^[1] Clinical monitoring of this process relies on serial wound measurements to track reductions in length, width, and depth, which reflect effective tissue filling and contraction over successive weeks.^[17] Biomarker analysis of wound exudate further aids assessment, with elevated vascular endothelial growth factor (VEGF) levels signaling robust angiogenesis and active granulation tissue development.^[1] Favorable outcomes involve a seamless transition to mature scar tissue by weeks 4 to 6, achieving sufficient tensile strength without significant contracture or deformity, thereby restoring functional integrity.^[46] Promoting factors include a moist wound environment, which enhances epithelial cell migration and prevents desiccation to accelerate granulation, as well as nutritional support with zinc for enzymatic reactions in collagen synthesis and vitamin C for hydroxylation of proline and lysine residues essential to matrix stability.^[47]^[48]

Pathological Conditions

Hypergranulation, also known as overgranulation, refers to the excessive proliferation of granulation tissue that protrudes above the wound surface, forming a raised, friable mass of red, shiny, and soft tissue.^[13] This condition commonly arises in wounds such as venous ulcers, burns, and pressure sores, affecting approximately 10-15% of burn patients in clinical settings.^[13] Key causes include excessive moisture in the wound environment, which promotes unchecked fibroblast and endothelial cell activity; presence of foreign bodies like dressing residues that trigger persistent inflammation; and mechanical irritation or friction that sustains cytokine release.^[1] Additionally, underlying infections can exacerbate the process by recruiting excessive inflammatory cells, leading to overproduction of growth factors.^[1] The consequences are significant, as the exuberant tissue barrier prevents epithelial cell migration across the wound bed, thereby delaying closure and increasing the risk of prolonged healing times—often extending median recovery to 45 days or more in affected cases.^[13] In contrast, hypogranulation involves inadequate formation of granulation tissue, resulting in a deficient vascular and matrix scaffold that stalls the proliferative phase of healing.^[1] This is particularly prevalent in chronic wounds associated with diabetes mellitus and ischemia, where hyperglycemia impairs fibroblast function and endothelial cell proliferation through glucose toxicity, leading to reduced collagen deposition and poor tissue fill.^[49] Ischemic conditions further exacerbate this by limiting oxygen delivery, which hinders angiogenesis and extracellular matrix synthesis.^[1] Bacterial biofilms, common in 60-80% of chronic wounds, interfere by promoting a sustained inflammatory state that downregulates vascular endothelial growth factor (VEGF) expression, thereby diminishing new vessel formation and granulation tissue development.^[50] The outcome is stalled wound progression, increased susceptibility to infection, and chronic non-healing ulcers that may persist for weeks beyond normal timelines, such as an additional 2 weeks in biofilm-challenged models.^[51] Related pathologies highlight variations in granulation tissue dynamics. Pyogenic granuloma, a benign vascular neoplasm also termed lobular capillary hemangioma, represents an excessive localized proliferation within granulation tissue, often triggered by minor trauma, hormonal influences, or medications like retinoids.^[7] It manifests as a rapidly growing, pedunculated, friable red papule prone to ulceration and bleeding, mimicking overgranulation but confined to skin or mucosa without broader wound involvement.^[7] Granuloma annulare, a dermatological granulomatous disorder, features annular plaques from palisaded histiocytic inflammation and mucin deposition in the dermis, distinct from the vascular-rich granulation tissue of wound repair as it involves collagen degeneration rather than proliferative healing.^[52] Unlike these, keloids arise from fibrotic over-remodeling in the post-granulation remodeling phase, characterized by excessive type I collagen accumulation and disorganized extracellular matrix beyond the original wound margins, driven by persistent TGF-β1 signaling and fibroblast hyperactivity.^[53] This contrasts with the temporary, organized type III collagen scaffold of granulation tissue, resulting in raised, pruritic scars that expand indefinitely.^[53]

Diagnostic and Management Approaches

Diagnostic approaches for granulation tissue primarily involve non-invasive imaging and invasive sampling to evaluate wound status, tissue quality, and potential complications. Wound photography, often enhanced by digital image analysis, allows for objective assessment of granulation tissue color, area, and percentage coverage, serving as a reliable tool for monitoring healing progression and quality.^[54] High-frequency ultrasound is utilized to measure wound depth, granulation tissue thickness, and vascularity, providing insights into tissue perfusion and structural changes during repair.^[55] In cases where atypical presentation raises suspicion, biopsy enables histological examination to confirm granulation tissue characteristics and rule out underlying malignancy, such as ulcerating carcinoma mimicking granulation.^[56] Additionally, analysis of wound fluid biomarkers, including matrix metalloproteinase (MMP) levels, helps gauge inflammatory activity and healing potential, with elevated MMPs indicating impaired granulation formation in chronic wounds.^[57] Management strategies aim to foster optimal granulation tissue development by addressing barriers to healing and enhancing the wound microenvironment. Debridement, through mechanical or autolytic methods, removes necrotic debris and biofilm, thereby reducing bacterial load and promoting the formation of healthy granulation tissue essential for subsequent repair phases.^[58] Moist wound environments are maintained using hydrocolloid dressings, which facilitate autolytic debridement, support angiogenesis, and accelerate granulation tissue proliferation compared to dry conditions.^[59] Advanced therapies further optimize granulation by improving vascular supply and cellular activity. Negative pressure wound therapy (NPWT) applies sub-atmospheric pressure to enhance perfusion—demonstrating up to a four-fold increase in blood flow in experimental models—and stimulates robust granulation tissue formation while minimizing edema.^[60] Topical application of growth factors, such as becaplermin (recombinant platelet-derived growth factor), has been shown in clinical trials to increase granulation tissue volume and promote complete wound closure in diabetic ulcers with adequate perfusion.^[61] Recent advances include stem cell-based therapies, where mesenchymal stem cells applied topically have demonstrated improved granulation tissue integration and faster wound closure in chronic ulcers, as evidenced by clinical evaluations including a 2024 meta-analysis showing significant reductions in ulcer area and enhanced healing rates.^[62] For infection control, which can hinder granulation, silver-impregnated dressings effectively manage critical colonization and infected wounds by reducing microbial burden without impeding tissue repair.^[63]

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Based on Clinical Research Matrix Metalloprotease (MMP) Inhibitors ...
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Silver dressings as an alternative safe and effective for treating infected wounds and/or in situations of critical colonization. There are already evidence of ...