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Pannus
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Pannus is an abnormal layer of fibrovascular tissue or granulation tissue. Common sites for pannus formation include over the cornea, over a joint surface (as seen in rheumatoid arthritis), or on a prosthetic heart valve.[1] Pannus may grow in a tumor-like fashion, as in joints where it may erode articular cartilage and bone.
In common usage, the term pannus is often used to refer to a panniculus (a hanging flap of tissue).
Pannus in rheumatoid arthritis
[edit]The term "pannus" is derived from the Latin for "tablecloth". Chronic inflammation and exuberant proliferation of the synovium leads to formation of pannus and destruction of cartilage, bone, tendons, ligaments, and blood vessels.[2] Pannus tissue is composed of aggressive macrophage- and fibroblast-like mesenchymal cells, macrophage-like cells and other inflammatory cells that release collagenolytic enzymes.[3]
In people suffering from rheumatoid arthritis, pannus tissue eventually forms in the joint affected by the disease, causing bony erosion and cartilage loss via release of IL-1, prostaglandins, and substance P by macrophages.
Pannus in ophthalmology
[edit]In ophthalmology, pannus refers to the growth of blood vessels into the peripheral cornea. In normal individuals, the cornea is avascular. Chronic local hypoxia (such as that occurring with overuse of contact lenses) or inflammation may lead to peripheral corneal vascularization, or pannus. Pannus may also develop in diseases of the corneal stem cells, such as aniridia. It is often resolved by peritomy.
References
[edit]- ^ Farlex Partner Medical Dictionary © Farlex 2012
- ^ Ranatunga, Sriya K M (2023-09-05). "Rheumatoid Arthritis (RA): Practice Essentials, Background, Pathophysiology". Medscape Reference. Retrieved 2024-08-08.
- ^ Furuzawa-Carballeda, J.; Macip-Rodríguez, P.M.; Cabral, A.R. (2008). "Osteoarthritis and rheumatoid arthritis pannus have similar qualitative metabolic characteristics and pro-inflammatory cytokine response". Retrieved December 5, 2015.
Pannus
View on Grokipediafrom Grokipedia
Pannus is a medical term derived from Latin meaning "cloth," referring to an abnormal layer of fibrovascular tissue or granulation tissue that forms over normal structures in response to chronic inflammation or other pathological processes.[1][2] In its most common usages, pannus describes either the vascular opacity on the cornea associated with infections like trachoma, the invasive synovial tissue in rheumatoid arthritis that erodes joint cartilage and bone, the fibrotic tissue overgrowth on prosthetic heart valves,[3] or an overhanging apron of excess skin and fat on the abdomen following significant weight loss or obesity.[4][5][6]
In ophthalmology, corneal pannus involves subepithelial neovascularization of the peripheral cornea, often graded as new (active vessels) or old (scarred), and serves as a clinical sign of ongoing infection, particularly with Chlamydia trachomatis in trachoma-endemic areas, where it contributes to visual impairment if untreated.[4] This form arises from inflammatory exudate and infiltration, leading to superficial opacity and potential progression to central corneal involvement.[7]
In rheumatology, pannus is a hallmark of rheumatoid arthritis (RA), where persistent synovitis transforms the synovial membrane into invasive, hypervascular tissue that produces enzymes and cytokines (such as IL-1 and TNF-α), promoting osteoclast activation and bone resorption, directly degrading cartilage and subchondral bone to cause erosions, pain, swelling, and eventual joint deformity or ankylosis.[5] Formation begins with synovial hyperplasia and neoangiogenesis, typically affecting small joints like those in the hands and feet early in the disease, and is detectable via imaging modalities such as MRI or ultrasound.[5] Early intervention with disease-modifying antirheumatic drugs (DMARDs) can halt pannus progression and prevent irreversible damage.[1]
In the context of obesity or post-bariatric surgery, abdominal pannus—also termed panniculus—manifests as a pendulous mass of redundant skin and subcutaneous fat extending below the waistline, often graded by extent (e.g., reaching the mons pubis or knees), and leading to complications like intertrigo, infections, mobility limitations, and hygiene challenges due to moisture accumulation.[6][8] Surgical removal via panniculectomy is indicated for severe cases to alleviate symptoms, though it is distinct from cosmetic procedures like abdominoplasty.[6]
Etymology and Overview
Etymology
The term pannus originates from the Latin noun pannus, meaning "piece of cloth," "rag," or "bandage," evoking imagery of a draped or covering material. This etymological root was borrowed into English medical vocabulary to characterize pathological tissue proliferations that form veil-like or cloak-like layers over underlying structures.[9][10][11] In early medical literature, pannus appeared in descriptions of inflammatory ocular tissues, with the earliest known reference dating to the 9th century by the physician Hunayn ibn Ishaq (808–873 AD), who used the Arabic term sabal for vascular overgrowth on the cornea in trachoma cases, a concept later translated and adopted as pannus in Latin-influenced texts. By the early modern period, the term gained traction in European medicine for similar abnormal coverings, evolving from general inflammatory observations to more precise anatomical notations. Historical records indicate its application in 16th- and 17th-century surgical and ophthalmic writings to denote excrescences or growths resembling cloth-like adhesions.[12] The 19th century marked a refinement of pannus in specialized contexts, particularly in ophthalmology amid trachoma epidemics in Europe, where it specifically referred to fibrovascular tissue invading the cornea, causing opacity and vascularization, as documented in clinical reports from British and continental physicians studying infectious eye diseases. This period's texts, influenced by microscopic advancements, solidified pannus as a descriptor for progressive, cloth-like corneal encroachment in trachoma-related pathology.[12][13] With 20th-century progress in pathology and surgery, pannus transitioned to broader applications: in rheumatology, it denoted hyperplastic synovial tissue eroding joints in rheumatoid arthritis, as detailed in early histopathological studies from the 1920s onward; in cardiology, it described fibrous overgrowth on prosthetic heart valves, emerging in literature following the 1960s advent of valve replacements. In plastic and bariatric surgery, the term has also been applied since the mid-20th century to describe pendulous abdominal tissue following significant weight loss, often as panniculus, retaining the "cloth-like" connotation for draped excess skin. These modern usages retained the original connotation of an invasive or covering tissue while adapting to specialized fields.[14][15][16]General Definition
In pathology, pannus refers to an abnormal proliferation of fibrous, vascular, or granulation tissue that forms a covering or layer over normal anatomical structures, often arising in an inflammatory context. This tissue typically consists of a mix of fibroblasts, inflammatory cells, and new blood vessels, creating a sheet-like growth that adheres to and obscures underlying surfaces.[10][17] Common characteristics of pannus include its invasive growth pattern, whereby it extends into adjacent tissues, potentially causing erosion and degradation of normal structures such as cartilage or endothelium.[18] It is frequently linked to chronic inflammation or host responses to foreign bodies, like prosthetic implants, promoting ongoing tissue remodeling.[19] The term derives from the Latin pannus, meaning "cloth" or "rag," evoking the appearance of a draped, membranous layer.[1] In the context of obesity or post-bariatric surgery, pannus—also termed panniculus—refers to a pendulous apron of excess skin and subcutaneous fat extending below the waistline.[6] Pannus is distinct from a granuloma, which manifests as a localized nodule of aggregated macrophages and other immune cells, and from fibrosis, involving diffuse scarring through excessive collagen deposition without significant vascular proliferation or inflammatory activity.[20][21]Pannus in Rheumatology
Formation in Rheumatoid Arthritis
In rheumatoid arthritis (RA), pannus formation begins with autoimmune-mediated inflammation targeting the synovial membrane, where immune complexes such as anti-citrullinated protein antibodies (ACPAs) activate macrophages and T cells, triggering the release of proinflammatory cytokines including tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1).[22] These cytokines promote synovial hyperplasia by stimulating the proliferation and activation of fibroblast-like synoviocytes (FLS) and macrophages, leading to an influx of inflammatory cells and neovascularization within the synovium.[23] This initial phase establishes a hyperplastic, aggressive tissue mass known as pannus, characterized by its tumor-like invasive properties.[22] The progression of pannus unfolds in distinct stages, starting with early synovial thickening due to cellular hyperplasia and edema, which expands the synovial lining and creates a villous architecture.[23] As inflammation intensifies, the pannus advances to invade the underlying articular cartilage through enzymatic degradation and direct cellular migration, followed by extension into subchondral bone, resulting in erosions.[24] Bone erosions, resulting from pannus invasion, can appear within weeks to months after RA symptom onset, affecting approximately 50-70% of untreated patients within the first year.[24] Central to the destructive process are invasive synovial fibroblasts within the pannus, which exhibit tumor-like behavior and produce and secrete matrix metalloproteinases (MMPs) such as MMP-1, MMP-3, and MMP-13.[25] These enzymes, upregulated by TNF-α and IL-1 signaling, specifically target collagen and proteoglycans in the extracellular matrix, facilitating the pannus's destructive advancement.[25] Macrophages within the pannus further amplify this process by contributing additional MMPs and cytokines, sustaining the inflammatory microenvironment.[22]Pathological Effects on Joints
In rheumatoid arthritis (RA), the pannus tissue invades the joint structures, releasing matrix metalloproteinases (MMPs) such as collagenases that degrade extracellular matrix components, including cartilage and subchondral bone.[26] These enzymes, primarily produced by synovial fibroblasts and macrophages within the pannus, as well as activated chondrocytes in the cartilage, facilitate focal erosions at the bone-cartilage interface, resulting in progressive cartilage loss and visible joint space narrowing on plain radiographs.[25][27] This enzymatic degradation and direct invasion by pannus lead to key clinical manifestations, including chronic joint pain from inflamed synovium and eroded tissues, reduced range of motion due to ligamentous instability, and characteristic deformities such as ulnar deviation of the fingers at the metacarpophalangeal joints.[28][29] Pannus-driven destruction accounts for the majority of irreversible joint damage in RA, with erosions and cartilage breakdown compromising joint integrity and function over time.[30] In advanced stages, unchecked pannus activity can culminate in ankylosis, or bony fusion of the affected joints, severely limiting mobility and leading to permanent disability.[27] Notably, pannus tissue often persists as an inactive, fibrotic remnant even after systemic inflammation resolves, contributing to ongoing structural deformity without active synovitis.[17] This arises from the initial synovial proliferation in RA, where hyperplastic synovium transforms into invasive pannus.[31]Pannus in Ophthalmology
Corneal Vascularization
Corneal pannus, also known as superficial corneal neovascularization, manifests as abnormal ingrowth of fibrovascular tissue from the limbus onto the peripheral cornea. This tissue typically appears as a wedge-shaped opacity originating at the corneoscleral junction, with fine, superficial blood vessels branching perilimbally and potentially extending toward the central cornea. The opacity often presents as a grayish or hazy area, separating the epithelium from Bowman's layer, and may form focal, regional, or diffuse patterns depending on the extent of involvement.[32][33][34] The optical consequences of corneal pannus primarily involve diminished corneal transparency due to the vascular structures and associated fibrosis, which scatter light and induce scarring. This leads to varying degrees of visual impairment, particularly when vessels encroach on the visual axis, causing reduced acuity and potential permanent vision loss in advanced cases. Severity is often graded by the extent of involvement: for instance, Stage 1 is limited to limbal or peripheral opacity without central extension (e.g., not reaching the central 5 mm zone), while Stage 3 features extensive pupillary or central involvement with complete opacification and vascularization across the cornea.[35][36][37] Histologically, corneal pannus consists of proliferating vascular endothelial cells forming new capillaries within a fibrovascular matrix, accompanied by fibroblast activation and collagen deposition that contributes to the tissue's opacity and rigidity. Unlike acute inflammatory processes, mature pannus typically shows minimal leukocyte infiltration, though active lesions may exhibit some inflammatory cell presence without dominating the overall composition. This fibrocollagenous structure underscores the chronic, reparative nature of the ingrowth.[32][38][39]Associated Conditions and Causes
Ophthalmic pannus primarily arises from chronic inflammation that disrupts the cornea's natural avascularity, allowing vascular ingrowth from the limbus. One of the leading causes is trachoma, an infectious disease caused by repeated exposure to Chlamydia trachomatis, which is highly prevalent in endemic regions of Africa, the Middle East, and parts of Asia. In untreated cases of trachoma, chronic conjunctival inflammation leads to corneal pannus, particularly in hyperendemic areas where repeated infections scar the ocular surface over years.[40][41] Other primary triggers include prolonged contact lens overuse, which induces corneal hypoxia and epithelial stress, and chemical burns that damage the limbal barrier and provoke angiogenic responses.[42][43] Secondary associations with pannus formation include severe ocular surface disorders such as Stevens-Johnson syndrome, where immune-mediated mucocutaneous reactions cause limbal stem cell deficiency and subsequent vascular invasion of the cornea. Rosacea keratitis, characterized by meibomian gland dysfunction and chronic lid margin inflammation, can also promote peripheral corneal neovascularization as part of its corneal involvement. Additionally, post-surgical complications, such as recurrence after pterygium excision, may result in fibrovascular pannus regrowth at the surgical site due to residual inflammatory stimuli.[44][45][46] Key risk factors exacerbating pannus development encompass environmental and physiological elements that heighten ocular surface vulnerability. Ultraviolet (UV) exposure contributes by inducing chronic epithelial irritation, particularly in outdoor workers or those in high-altitude regions. Dry eye disease, often from aqueous deficiency or evaporative loss, fosters persistent inflammation that can tip the angiogenic balance toward neovascularization.[35][47]Pannus in Cardiology
Development on Prosthetic Valves
Pannus formation on prosthetic heart valves arises as an exaggerated biological reaction of host tissue to the foreign prosthetic material, characterized by the proliferation of fibroblasts and myofibroblasts that deposit extracellular matrix components, such as collagen and elastic fibers.[48][49] This fibrotic ingrowth typically originates in the subvalvular or periannular regions, beginning from the ventricular aspect of the valve and progressively extending toward the leaflets over time.[50][51] The process is driven by a chronic inflammatory response, involving neointimal hyperplasia similar to that seen in vascular grafts, and can lead to restricted leaflet motion without significant thrombus involvement.[51][52] The incidence of pannus formation causing prosthetic obstruction is similar in mechanical and bioprosthetic valves,[53] particularly noted in mechanical bileaflet designs such as the St. Jude Medical valve implanted in the aortic position, where high shear stress from turbulent blood flow exacerbates tissue overgrowth and healing responses.[54][55] In bioprosthetic valves, pannus formation occurs later in their lifespan, often synergizing with degenerative calcification that accelerates leaflet stiffening and obstruction through shared inflammatory pathways.[56][15] The development generally unfolds over several years post-implantation, with most cases manifesting 5 years or more after surgery, though earlier onset within 2-5 years has been reported in susceptible patients.[57][58] The incidence of pannus contributing to prosthetic valve dysfunction ranges from 1% to 5%, representing a notable but underrecognized cause among obstructive complications, and it often remains subclinical until significant hemodynamic compromise occurs, such as when echocardiography reveals a mean transvalvular gradient exceeding 10 mmHg.[48][59] This delayed detection underscores the chronic, insidious nature of pannus ingrowth compared to more acute etiologies like thrombosis.[3]Clinical Implications and Diagnosis
Pannus formation on prosthetic heart valves manifests through progressive obstruction, leading to valvular stenosis or regurgitation that elicits symptoms of heart failure, such as dyspnea and fatigue. These symptoms typically emerge gradually, often years after valve implantation, due to the chronic nature of pannus as fibrotic tissue overgrowth interfering with leaflet motion. Complications include increased morbidity and mortality from untreated obstruction, as well as a risk of systemic embolization if portions of the pannus become mobile, though this is less common than with thrombus.[3][53][60] Diagnosis relies on multimodal imaging to confirm obstruction and characterize the lesion. Transthoracic echocardiography serves as the initial assessment, evaluating hemodynamic parameters like transvalvular gradients, but it is limited by acoustic shadowing from the prosthesis. Transesophageal echocardiography provides superior resolution, identifying fixed echodense masses indicative of pannus versus more mobile, lower-density thrombi, with masses smaller than 0.8 cm² associated with lower risks in related treatments. Cinefluoroscopy complements this by visualizing restricted leaflet excursion in real-time, confirming mechanical obstruction without directly identifying tissue type.[3][53][60] Computed tomography angiography offers critical differentiation by quantifying lesion density, with pannus exhibiting higher attenuation values of ≥145 Hounsfield units (HU), compared to thrombus typically below 90 HU.[61] This density distinction guides management, as pannus is less responsive to anticoagulation and typically necessitates surgical intervention, whereas thrombus may resolve with thrombolysis. Challenges arise from potential coexistence of pannus and thrombus in up to 45% of cases, particularly in mitral prostheses, and imaging artifacts in older valves, often requiring surgical exploration for definitive confirmation.[3][53][60]Abdominal Pannus
Characteristics and Formation
Abdominal pannus, also known as apron belly or mother's apron, refers to a pendulous apron of excess adipose tissue and dermis that overhangs the lower abdomen and extends below the waistline.[62] This condition manifests as a layer of skin and fat that hangs downward, often varying in size from a mild overhang to a significant mass reaching the thighs or knees.[63] Physically, it typically presents with stretched skin that may exhibit striae (stretch marks), discoloration due to chronic irritation, and a soft, mobile texture, though in advanced cases it can become firmer from fibrosis.[8] The extent of abdominal pannus is commonly graded on a scale of 1 to 5 based on how far the tissue extends downward, as outlined by the American Society of Plastic Surgeons. Grade 1 involves coverage of the hairline and mons pubis without reaching the genitals; Grade 2 extends to cover the genitals and upper thigh crease; Grade 3 reaches the upper thigh; Grade 4 covers the mid-thigh; and Grade 5 extends to the knees or below.[64] This classification helps assess the severity and impact on mobility, with higher grades indicating greater overhang and potential for skin folding. Formation of abdominal pannus arises primarily from factors that lead to skin inelasticity and fat redistribution, including rapid weight loss, pregnancy, and aging. Rapid weight loss, such as that following bariatric surgery where individuals lose more than 50 kg, stretches the skin beyond its elastic capacity, resulting in redundant tissue that fails to retract.[65] Pregnancy contributes by causing abdominal distension from fetal growth, leading to permanent skin laxity post-delivery, especially in multiparous women.[62] Aging exacerbates this through natural collagen degradation and hormonal shifts that promote central fat accumulation and reduced skin tone.[63] Abdominal pannus is particularly prevalent among individuals with obesity (BMI >30 kg/m²), affecting a substantial proportion of this population, and is more common in women due to gynecological factors like pregnancy and estrogen-influenced fat distribution patterns.[8] For instance, in adolescents undergoing bariatric surgery—a group representative of severe obesity—over 90% present with an abdominal pannus preoperatively.[66]Health Risks and Management
Abdominal pannus poses several health risks, primarily due to its mechanical and dermatological effects in individuals with severe obesity. Chronic infections, such as intertrigo, are common in the skinfolds beneath the pannus, where moisture and friction promote bacterial and fungal overgrowth, leading to recurrent rashes and ulceration if untreated.[67] Hygiene challenges arise from the difficulty in cleaning and drying the area, exacerbating skin breakdown and increasing the risk of secondary infections.[67] Additionally, the excessive weight of the pannus can cause back pain by altering posture and weight distribution, contributing to chronic musculoskeletal strain and reduced mobility.[68] The pannus also heightens the risk of ventral hernias, as the overhanging tissue weakens the abdominal wall and promotes intra-abdominal pressure imbalances, with obesity identified as an independent risk factor for hernia development.[69] Management of abdominal pannus begins with conservative approaches aimed at symptom relief and risk mitigation. Weight maintenance through diet and exercise is foundational, as sustained weight loss can reduce pannus size and alleviate associated complications.[8] Compression garments provide support to minimize friction, improve hygiene, and reduce pain during movement, often recommended as a first-line intervention.[70] For persistent issues, surgical options include panniculectomy, which removes excess skin and fat (typically more than 2 kg of tissue) to address functional impairments like infections or mobility limitations, rather than cosmetic concerns.[71] Abdominoplasty may be performed for cosmetic improvement but does not tighten underlying muscles unless combined with reconstructive elements.[8] Intervention criteria for surgical management, particularly for insurance coverage like Medicare, require documentation of medical necessity. Coverage is typically granted when the pannus extends below the pubis, causing chronic rashes or intertrigo unresponsive to at least three months of conservative treatment, or when it impairs mobility and daily activities.[72] Functional criteria also include evidence of recurrent infections, ulceration, or pain limiting ambulation, ensuring procedures are not deemed cosmetic.[73]References
- https://en.wiktionary.org/wiki/pannus