Materiały źródłowe

• #1 A brief review on classification of oral ulcerative lesions – JOOO

  https://www.joooo.org/html-article/13245

  Ulcers are among the most common mouth lesions. The epidemiology varies, depending upon the cause of the ulceration. Ulcers and erosions are the final common manifestation of a spectrum of conditions ranging from autoimmune diseases to neoplastic, traumatic, infectious lesions, nutritional deficiencies and drug reactions, and they represent a diagnostic challenge for dental practitioners. […] […] Oral ulcer or ulceration is characterized by the complete loss of epithelium accompanied by a variable loss of the underlying connective tissue, resulting in a crateriform appearance, which may be augmented by oedema andor a proliferation of the surrounding tissue. […] […] Ulcers which commonly occur in the mouth have causes that may range from minor irritation to malignancies and systemic diseases. Innocent solitary ulcerations, which result from trauma and infections, must be distinguished from squamous cell carcinomas, which also typically present as solitary ulcers. Multiple oral ulcers may be classified as acute, recurrent and/or chronic. Various classification system that has been given under which ulcers were classified. […]

• #2 Oral Aphthous: Pathophysiology, Clinical Aspects and Medical Treatment

  https://archrazi.areeo.ac.ir/article_125377.html

  Oral aphthous can appear alone or secondary to numerous distinct disease processes. […] The pathophysiology of oral aphthous ulcers remains unclear but various bacteria are part of its microbiology. […] The pathogenesis of recurrent aphthosis stomatitis (RAS) remains poorly defined. It likely involves a predominantly cell-mediated inflammation involving T-cells and TNF- (tumor necrosis factor-alpha) production. […] Light and electron-microscope examination of oral aphthous ulcers showed a penetrating, early, lympho-monocyte infiltration of the epithelium. […] According to a study by Lehner, under light microscopy, oral ulcer epithelium showed considerable intercellular edema and degenerative changes. […] There was epithelial hyperplasia and only the basement membrane adjacent to the ulcer was affected, the rest of the basement membrane appeared intact.

• #3 Oral Aphthous: Pathophysiology, Clinical Aspects and Medical Treatment

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8934078/

  The pathogenesis of recurrent aphthosis stomatitis (RAS) remains poorly defined. It likely involves a predominantly cell-mediated inflammation involving T-cells and TNF- (tumor necrosis factor-alpha) production. […] Light and electron-microscope examination of oral aphthous ulcers showed a penetrating, early, lympho-monocyte infiltration of the epithelium. […] According to a study by Lehner, under light microscopy, oral ulcer epithelium showed considerable intercellular edema and degenerative changes. […] There was epithelial hyperplasia and only the basement membrane adjacent to the ulcer was affected, the rest of the basement membrane appeared intact. […] Mononuclear cells normally infiltrate the basal-cell and prickle-cell layers of the epidermis and they are most commonly lymphocytes and monocytes, but superficial to and immediately adjacent to the ulcer neutrophil polymorphs were also found.

• #4 Recurrent Aphthous Stomatitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK431059/

  Recurrent aphthous stomatitis (RAS) is a chronic oral mucosa inflammatory disorder with an uncertain etiology. […] The etiology of recurrent aphthous stomatitis remains imperfectly understood. The cause is believed to be multifactorial, involving a cell-mediated immunological reaction and a genetic predisposition. Histopathological changes are seen before ulceration occurs. Lymphocytes (mononuclear cells) infiltrate the oral epithelium, edema develops, and the keratinocytes (oral epithelial cells) undergo vacuolization and vasculitis. This results in localized swelling and later ulceration of the epithelium. Infiltration with neutrophils, lymphocytes, and plasma cells occurs before the epithelium heals and regenerates. The pathogenesis of RAS is a T-cell-mediated immunological reaction involving the inflammatory cytokine named tumor necrosis factor-alpha (TNF-). TNF- activates the chemotaxis of neutrophils, generating an acute inflammatory response and the expression of the major histocompatibility (MHC) complex.

• #5 Oral Aphthous: Pathophysiology, Clinical Aspects and Medical Treatment

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8934078/

  The pathogenesis of recurrent aphthosis stomatitis (RAS) remains poorly defined. It likely involves a predominantly cell-mediated inflammation involving T-cells and TNF- (tumor necrosis factor-alpha) production. […] Light and electron-microscope examination of oral aphthous ulcers showed a penetrating, early, lympho-monocyte infiltration of the epithelium. […] According to a study by Lehner, under light microscopy, oral ulcer epithelium showed considerable intercellular edema and degenerative changes. […] There was epithelial hyperplasia and only the basement membrane adjacent to the ulcer was affected, the rest of the basement membrane appeared intact. […] Mononuclear cells normally infiltrate the basal-cell and prickle-cell layers of the epidermis and they are most commonly lymphocytes and monocytes, but superficial to and immediately adjacent to the ulcer neutrophil polymorphs were also found.

• #6 Oral Aphthous: Pathophysiology, Clinical Aspects and Medical Treatment

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8934078/

  The pathogenesis of recurrent aphthosis stomatitis (RAS) remains poorly defined. It likely involves a predominantly cell-mediated inflammation involving T-cells and TNF- (tumor necrosis factor-alpha) production. […] Light and electron-microscope examination of oral aphthous ulcers showed a penetrating, early, lympho-monocyte infiltration of the epithelium. […] According to a study by Lehner, under light microscopy, oral ulcer epithelium showed considerable intercellular edema and degenerative changes. […] There was epithelial hyperplasia and only the basement membrane adjacent to the ulcer was affected, the rest of the basement membrane appeared intact. […] Mononuclear cells normally infiltrate the basal-cell and prickle-cell layers of the epidermis and they are most commonly lymphocytes and monocytes, but superficial to and immediately adjacent to the ulcer neutrophil polymorphs were also found.

• #7 Oral Aphthous: Pathophysiology, Clinical Aspects and Medical Treatment

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8934078/

  An immunofluorescent examination couldn’t detect specific globulin binding to salivary gland tissue in the oral aphthous lesion. […] Major aphthous ulcers do not differ much from minor aphthous ulcers, but they have an increase in the degree of severity of the pathological changes. […] There were no vascular abnormalities and fibrinous necrosis noticed in recurrent oral ulcers. […] A three-fold rise in mast cells was found in recurrent oral aphthous, in contrast to a decreased count in non-specific ulcers. […] Mast cell count was present in all three groups of oral ulcers when it was compared with that in other oral lesions and normal tissue. […] Leukocytes have a normal chemotactic function in oral aphthosis but in Behcet’s disease, they showed hyperactive function. […] There’s a chance that a few immunologically arbitrated mechanisms are playing an important role in the pathogenesis of oral aphthosis. […] It may be due to an unopposed or excessive production of IL (interleukin)-1 or IL-6, which is essential for its development, a concept that may explain why ulceration worsens after local injury, or cessation of smoking, or both.

• #8 Oral Aphthous: Pathophysiology, Clinical Aspects and Medical Treatment

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8934078/

  An immunofluorescent examination couldn’t detect specific globulin binding to salivary gland tissue in the oral aphthous lesion. […] Major aphthous ulcers do not differ much from minor aphthous ulcers, but they have an increase in the degree of severity of the pathological changes. […] There were no vascular abnormalities and fibrinous necrosis noticed in recurrent oral ulcers. […] A three-fold rise in mast cells was found in recurrent oral aphthous, in contrast to a decreased count in non-specific ulcers. […] Mast cell count was present in all three groups of oral ulcers when it was compared with that in other oral lesions and normal tissue. […] Leukocytes have a normal chemotactic function in oral aphthosis but in Behcet’s disease, they showed hyperactive function. […] There’s a chance that a few immunologically arbitrated mechanisms are playing an important role in the pathogenesis of oral aphthosis. […] It may be due to an unopposed or excessive production of IL (interleukin)-1 or IL-6, which is essential for its development, a concept that may explain why ulceration worsens after local injury, or cessation of smoking, or both.

• #9

  https://journals.lww.com/apmd/fulltext/2017/14040/recurrent_aphthous_ulcers___still_a_challenging.3.aspx

  It is likely that immunologically mediated mechanism is involved in the etiopathogenesis of RAU. It may be due to excessive production of interleukin 1 (IL-1) or IL-6. […] The histopathological changes seen in the preulcerative phase include infiltration of lymphocytic cells in the epithelium. The keratinocyte vacuolization and focal vasculitis lead to edema which ulcerates and is infiltrated with neutrophils, lymphocytes, and plasma cells. There is cell-mediated immune response with involvement of T-cells with generation of tumor necrosis factor alpha (TNF-) from these cells and mast cells and macrophages. […] TNF- is an important inflammatory cytokine which has a chemotactic action on neutrophil, so causing acute inflammation and expression of major histocompatibility complexes. It results in the targeting of epithelial cells by CD8 T-cells. […] Other cytokines implicated are IL-2, IL-10 or IL-1, and IL-6. The gamma delta T-lymphocytes may play role in an antibody-dependent cell-mediated cytotoxic reaction toward the oral mucosal layer for ulcer formation.

• #10 Recurrent Aphthous Stomatitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK431059/

  Recurrent aphthous stomatitis (RAS) is a chronic oral mucosa inflammatory disorder with an uncertain etiology. […] The etiology of recurrent aphthous stomatitis remains imperfectly understood. The cause is believed to be multifactorial, involving a cell-mediated immunological reaction and a genetic predisposition. Histopathological changes are seen before ulceration occurs. Lymphocytes (mononuclear cells) infiltrate the oral epithelium, edema develops, and the keratinocytes (oral epithelial cells) undergo vacuolization and vasculitis. This results in localized swelling and later ulceration of the epithelium. Infiltration with neutrophils, lymphocytes, and plasma cells occurs before the epithelium heals and regenerates. The pathogenesis of RAS is a T-cell-mediated immunological reaction involving the inflammatory cytokine named tumor necrosis factor-alpha (TNF-). TNF- activates the chemotaxis of neutrophils, generating an acute inflammatory response and the expression of the major histocompatibility (MHC) complex.

• #11

  https://journals.lww.com/apmd/fulltext/2017/14040/recurrent_aphthous_ulcers___still_a_challenging.3.aspx

  It is likely that immunologically mediated mechanism is involved in the etiopathogenesis of RAU. It may be due to excessive production of interleukin 1 (IL-1) or IL-6. […] The histopathological changes seen in the preulcerative phase include infiltration of lymphocytic cells in the epithelium. The keratinocyte vacuolization and focal vasculitis lead to edema which ulcerates and is infiltrated with neutrophils, lymphocytes, and plasma cells. There is cell-mediated immune response with involvement of T-cells with generation of tumor necrosis factor alpha (TNF-) from these cells and mast cells and macrophages. […] TNF- is an important inflammatory cytokine which has a chemotactic action on neutrophil, so causing acute inflammation and expression of major histocompatibility complexes. It results in the targeting of epithelial cells by CD8 T-cells. […] Other cytokines implicated are IL-2, IL-10 or IL-1, and IL-6. The gamma delta T-lymphocytes may play role in an antibody-dependent cell-mediated cytotoxic reaction toward the oral mucosal layer for ulcer formation.

• #12 Pathophysiology of Mouth Ulcers

  https://www.ijpsjournal.com/article/Pathophysiology+of+Mouth+Ulcers

  Mouth ulcers, also known as aphthous stomatitis, are common, painful lesions that affect the mucosal surfaces of the oral cavity. Their pathophysiology is complex, involving genetic, immunological, and environmental factors. […] Although the exact cause remains unclear, dysregulation of the immune system plays a central role. Inflammatory responses are triggered by the activation of T lymphocytes, which lead to the release of cytokines, resulting in epithelial cell damage and ulcer formation. Genetic predisposition, stress, trauma, nutritional deficiencies (especially of B vitamins, folic acid, and iron), and microbial factors have all been implicated as contributing factors. […] The local tissue response is characterized by an imbalance between pro-inflammatory and anti-inflammatory mediators, with the upregulation of cytokines such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-?), and interferon-gamma (IFN-?). This results in increased vascular permeability, edema, and neutrophil infiltration, which further exacerbate the lesion.

• #13 Recurrent Aphthous Stomatitis – Dental Disorders – MSD Manual Professional Edition

  https://www.msdmanuals.com/professional/dental-disorders/symptoms-of-dental-and-oral-disorders/recurrent-aphthous-stomatitis

  Etiology is unclear, but RAS tends to run in families. The damage is predominately T-cell mediated. Cytokines, such as IL-2, IL-10, and particularly TNF-alpha, play a role. […] Some patients with food allergies may also have RAS and certain foods may exacerbate symptoms (eg, chocolate, peanuts, eggs). However, there are no studies directly linking food allergy as the cause of RAS. […] Diagnosis is based on appearance and on exclusion because there are no definitive histologic features or laboratory tests. […] Similar recurrent episodes, often with multiple ulcers, can occur with Behet disease, inflammatory bowel disease, celiac disease, HIV infection, PFAPA (periodic fevers with aphthous stomatitis, pharyngitis, and adenitis) syndrome, and nutritional deficiencies; these conditions generally have systemic symptoms and signs.

• #14 Aphthous Ulcers: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/867080-overview

  Patients with active RAS have an increased proportion of gamma-delta T cells compared with control subjects and patients with inactive RAS. Gamma-delta T cells may be involved in antibody-dependent, cell-mediated cytotoxicity (ADCC). […] Cross-reactivity between a streptococcal 60- to 65-kd heat shock protein (hsp) and the oral mucosa has been demonstrated, and significantly elevated levels of serum antibodies to hsp are found in patients with RAS. […] RAS thus may be a T cell-mediated response to antigens of S sanguinis, which cross-react with the mitochondrial hsp and induce oral mucosal damage. […] RAS patients have an anomalous activity of the toll-like receptor TLR2 pathway that probably influences the stimulation of an abnormal Th1 immune response. […] A literature review by Rahimi et al indicated that persons with RAS have a significantly higher neutrophil-to-lymphocyte ratio (NLR) than do individuals without the condition.

• #15 Recurrent Aphthous Stomatitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK431059/

  It has also been suggested that the T-cell-mediated reaction seen in RAS is in response to Streptococcus sanguis antigens that cross-react with mitochondrial heat shock proteins, causing damage to the oral mucosa. […] There is a genetic predisposition to RAS; a family history of the condition is seen in 24% to 46% of patients. […] Local trauma predisposes to recurrent aphthous stomatitis in susceptible individuals or those with a hereditary predisposition to the disease. […] Hematinic (iron, folic acid, or vitamin B12) and zinc deficiencies have been demonstrated in some patients with recurrent aphthous stomatitis. […] HIV patients have reduced CD4 lymphocyte and elevated CD8 lymphocyte levels, predisposing them to RAS.

• #16 Aphthous Ulcers: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/867080-overview

  The etiology of RAS is still unknown; the condition may in fact manifest from a group of disorders of quite different etiologies rather than from a single entity. […] Immune mechanisms appear to be at play in persons with a genetic predisposition to oral ulceration. […] The genetic basis for some RAS is shown by a positive family history in about one-third of patients with RAS; an increased frequency of human leukocyte antigen (HLA) types A2, A11, B12, and DR2; and susceptibility to RAS, which segregates in families in association with HLA haplotypes. RAS probably involves cell-mediated mechanisms, but the precise immunopathogenesis remains unclear. […] Phagocytic and cytotoxic T cells probably aid in destruction of oral epithelium, with this destruction directed and sustained by local cytokine release.

• #17 Aphthous Ulcers: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/867080-overview

  The etiology of RAS is still unknown; the condition may in fact manifest from a group of disorders of quite different etiologies rather than from a single entity. […] Immune mechanisms appear to be at play in persons with a genetic predisposition to oral ulceration. […] The genetic basis for some RAS is shown by a positive family history in about one-third of patients with RAS; an increased frequency of human leukocyte antigen (HLA) types A2, A11, B12, and DR2; and susceptibility to RAS, which segregates in families in association with HLA haplotypes. RAS probably involves cell-mediated mechanisms, but the precise immunopathogenesis remains unclear. […] Phagocytic and cytotoxic T cells probably aid in destruction of oral epithelium, with this destruction directed and sustained by local cytokine release.

• #18

  https://www.aaaai.org/allergist-resources/ask-the-expert/answers/old-ask-the-experts/aphthous

  The pathogensis of simple aphthous ulcers is unknown although there are theories that the ulcers are related to immune dysregulation. […] One study suggests genetic polymorphisms of the IL-10 gene, again supporting an immunologic mechanism. […] In summary, recurrent, simple aphthous ulceration is an idiopathic disorder with some suggestions of an immunologic mechanism but the pathogenesis is unknown. […] The results of currently performed studies indicate that genetically mediated disturbances of the innate and acquired immunity play an important role in the disease development. […] Factors that modify the immunologic response in RAS include: food allergies, vitamin and microelement deficiencies, hormonal and gastrointestinal disorders, some viral and bacterial infections, mechanical injuries and stress.

• #19

  https://www.aaaai.org/allergist-resources/ask-the-expert/answers/old-ask-the-experts/aphthous

  The results of this study suggest that certain SNPs of IL10 gene have association with predisposition of individuals to RAS. […] These findings confirm that mechanically induced injury of the oral mucosa may cause ulceration in people susceptible to aphthous stomatitis. […] Stressful life events were significantly associated with the onset of RAS episodes, but not with the duration of the RAS episodes. […] In patients with a history of RAS, stressful events may mediate changes involved in the initiation of new RAS episodes. Mental stressors are more strongly associated with RAS episodes than physical stressors.

• #20 Aphthous Stomatitis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1075570-overview

  Although the clinical characteristics of recurrent aphthous ulcer have been well defined, the precise etiology and the pathogenesis remain unclear. Many possibilities have been investigated. Recurrent aphthous ulcer is a multifactorial condition, and it is likely that immune-mediated destruction of the epithelium is the common factor in its pathogenesis. […] Immune dysregulation appears to play a significant role. Cytotoxic action of lymphocytes and monocytes on the oral epithelium may cause the ulceration, but the trigger remains unclear. Upon histologic analysis, recurrent aphthous ulcer consists of mucosal ulcerations with mixed inflammatory cell infiltrates. […] Researchers have disagreed about the role of microbes in the development of recurrent aphthous ulcers. The emphasis has been on a microbial agent as a primary pathogen or an antigenic stimulus. Numerous studies have failed to provide strong evidence to support the role of HSV, human herpesvirus (HHV), varicella-zoster virus (VZV), or cytomegalovirus (CMV) in the development of aphthous ulcers. […] Recurrent aphthous ulcer formation may be a T-cell-mediated response to antigens of Streptococcus sanguis that cross-react with the mitochondrial heat-shock proteins and induce damage to oral mucosa.

• #21 Aphthous Ulcers: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/867080-overview

  Patients with active RAS have an increased proportion of gamma-delta T cells compared with control subjects and patients with inactive RAS. Gamma-delta T cells may be involved in antibody-dependent, cell-mediated cytotoxicity (ADCC). […] Cross-reactivity between a streptococcal 60- to 65-kd heat shock protein (hsp) and the oral mucosa has been demonstrated, and significantly elevated levels of serum antibodies to hsp are found in patients with RAS. […] RAS thus may be a T cell-mediated response to antigens of S sanguinis, which cross-react with the mitochondrial hsp and induce oral mucosal damage. […] RAS patients have an anomalous activity of the toll-like receptor TLR2 pathway that probably influences the stimulation of an abnormal Th1 immune response. […] A literature review by Rahimi et al indicated that persons with RAS have a significantly higher neutrophil-to-lymphocyte ratio (NLR) than do individuals without the condition.

• #22 Recurrent Aphthous Stomatitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK431059/

  It has also been suggested that the T-cell-mediated reaction seen in RAS is in response to Streptococcus sanguis antigens that cross-react with mitochondrial heat shock proteins, causing damage to the oral mucosa. […] There is a genetic predisposition to RAS; a family history of the condition is seen in 24% to 46% of patients. […] Local trauma predisposes to recurrent aphthous stomatitis in susceptible individuals or those with a hereditary predisposition to the disease. […] Hematinic (iron, folic acid, or vitamin B12) and zinc deficiencies have been demonstrated in some patients with recurrent aphthous stomatitis. […] HIV patients have reduced CD4 lymphocyte and elevated CD8 lymphocyte levels, predisposing them to RAS.

• #23 Aphthous Ulcers: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/867080-overview

  Patients with active RAS have an increased proportion of gamma-delta T cells compared with control subjects and patients with inactive RAS. Gamma-delta T cells may be involved in antibody-dependent, cell-mediated cytotoxicity (ADCC). […] Cross-reactivity between a streptococcal 60- to 65-kd heat shock protein (hsp) and the oral mucosa has been demonstrated, and significantly elevated levels of serum antibodies to hsp are found in patients with RAS. […] RAS thus may be a T cell-mediated response to antigens of S sanguinis, which cross-react with the mitochondrial hsp and induce oral mucosal damage. […] RAS patients have an anomalous activity of the toll-like receptor TLR2 pathway that probably influences the stimulation of an abnormal Th1 immune response. […] A literature review by Rahimi et al indicated that persons with RAS have a significantly higher neutrophil-to-lymphocyte ratio (NLR) than do individuals without the condition.

• #24 Aphthous Stomatitis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1075570-overview

  Although the clinical characteristics of recurrent aphthous ulcer have been well defined, the precise etiology and the pathogenesis remain unclear. Many possibilities have been investigated. Recurrent aphthous ulcer is a multifactorial condition, and it is likely that immune-mediated destruction of the epithelium is the common factor in its pathogenesis. […] Immune dysregulation appears to play a significant role. Cytotoxic action of lymphocytes and monocytes on the oral epithelium may cause the ulceration, but the trigger remains unclear. Upon histologic analysis, recurrent aphthous ulcer consists of mucosal ulcerations with mixed inflammatory cell infiltrates. […] Researchers have disagreed about the role of microbes in the development of recurrent aphthous ulcers. The emphasis has been on a microbial agent as a primary pathogen or an antigenic stimulus. Numerous studies have failed to provide strong evidence to support the role of HSV, human herpesvirus (HHV), varicella-zoster virus (VZV), or cytomegalovirus (CMV) in the development of aphthous ulcers. […] Recurrent aphthous ulcer formation may be a T-cell-mediated response to antigens of Streptococcus sanguis that cross-react with the mitochondrial heat-shock proteins and induce damage to oral mucosa.

• #25 Oral Aphthous: Pathophysiology, Clinical Aspects and Medical Treatment

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8934078/

  According to Lehner, the Intra-nuclear inclusion bodies were found in 3 out of the 25 biopsies examined by electron microscopy. […] The affected nuclei were slightly larger and the nucleoli were uneven in shape. […] Inclusion bodies were not seen in the cytoplasm. […] Herpetiform ulcers differ from recurrent aphthous ulcers in that they showed epithelial vesicles and intra-nuclear inclusion bodies, suggesting a virus etiology. […] The immuno-fluorescent studies showed predominantly IgG and IgM binding only in autologous tissues from patients with aphthous ulcers. […] This reaction could indicate blood group antigens, trapped globulins due to the inflammatory reaction, non-immunological physicochemical binding of the fluorescent conjugate, or normal immunoglobulin transport through the oral mucosa.

• #26 Mouth ulcers | Better Health Channel

  https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/mouth-ulcers

  A mouth ulcer is the loss or erosion of part of the delicate tissue that lines the inside of the mouth (mucous membrane). […] There are many things that cause mouth ulcers. The most common cause is injury (such as accidentally biting the inside of your cheek). Other causes include aphthous ulceration, certain medications, skin rashes in the mouth, viral, bacterial and fungal infections, chemicals and some medical conditions. […] An ulcer that wont heal may be a sign of mouth cancer. […] Aphthous ulcers are recurring ulcers which affect around 20 per cent of the population. Although in most people there is no known cause for aphthous ulcers, in a small number of people these ulcers may be due to an underlying Vitamin B, folate or iron deficiency. […] Mouth ulcers can be caused by a wide range of factors including: Accidentally biting the inside of your cheek. Injury from a toothbrush (such as slipping while brushing). Constant rubbing against misaligned or sharp/broken teeth. Constant rubbing against dentures or braces. Burns from eating hot food. Irritation from strong antiseptics, such as a mouthwash. Aphthous ulcers. Viral infections such as the herpes simplex viral infection (cold sore virus). Reaction to certain medications. Skin rashes in the mouth (for example, lichen planus). Autoimmune diseases. Underlying Vitamin B2, folate or iron deficiency. Underlying gastrointestinal disease such as Crohns disease or coeliac disease. Mouth cancer. Ulcers may become worse during periods of stress, illness or extreme fatigue.

• #27 Mouth Ulcer: Causes, Symptoms, Diagnosis, and Treatment

  https://www.healthline.com/health/mouth-ulcers

  Mouth ulcers, which include canker sores, are small sores that develop within the mouth. There are no definite causes of mouth ulcers, but some injuries, allergies, or sensitivities may trigger them. […] Theres no definite cause behind mouth ulcers, but certain risk factors and triggers have been identified. […] Triggers include: minor mouth injury from dental work, hard brushing, sports injury, or an accidental bite, dental braces, toothpaste or mouthwash that contains sodium lauryl sulfate (SLS), an allergic response to oral bacteria, bacterial, viral, or fungal infections in the mouth, such as hand, foot, and mouth disease, sensitivities to acidic foods and beverages like strawberries, citrus fruits, pineapple, chocolate, and coffee, certain nutrient deficiencies, especially vitamin B9 (folate), vitamin B12, zinc, and iron, hormonal changes, such as those that occur during menstruation or pregnancy, emotional stress, lack of sleep.

• #28 Aphthous ulceration (aphthae, ulcers)

  https://dermnetnz.org/topics/aphthous-ulcer

  An aphthous ulcer is the most common ulcerative condition of the oral mucosa, and presents as a painful punched-out sore on oral or genital mucous membranes. […] The exact reason why aphthous ulcer develops is not yet clearly defined. Approximately 40% of people who get aphthous ulcers have a family history of aphthous ulcers. Current thinking is that the immune system is disturbed by some external factor and reacts abnormally against a protein in mucosal tissue. […] Factors that seem to trigger outbreaks of ulcers include: Emotional stress and lack of sleep, Mechanical trauma, for example, self-inflicted bite, Nutritional deficiency, particularly of vitamin B, iron, and folic acid, Certain foods, including chocolate, Certain toothpastes; this may relate to sodium laureth sulphate (the foaming component of toothpaste), Menstruation, Certain medications, including nicorandil, given for angina, Viral infections.

• #29 Mouth sores and ulcers (canker sores) | healthdirect

  https://www.healthdirect.gov.au/mouth-sores-and-ulcers

  Mouth ulcers are a type of sore which appears on the inside of your mouth. […] No one knows the exact cause of mouth ulcers, but there are several factors that can make you more likely to develop them. […] Mouth ulcers may be caused by: stress, anxiety or hormonal changes, any injury or damage to your mouth, such as from sharp teeth, dentures, or braces, a reaction to certain foods, including chocolate, peanuts, coffee, and gluten, toothpaste containing sodium lauryl sulphate (the foaming part of toothpaste), some infections and diseases, like coeliac disease, certain medicines and medical treatments, vitamin deficiencies. […] About 1 in 3 people who get mouth ulcers have family members who also get them.

• #30 Recurrent Aphthous Stomatitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK431059/

  It has also been suggested that the T-cell-mediated reaction seen in RAS is in response to Streptococcus sanguis antigens that cross-react with mitochondrial heat shock proteins, causing damage to the oral mucosa. […] There is a genetic predisposition to RAS; a family history of the condition is seen in 24% to 46% of patients. […] Local trauma predisposes to recurrent aphthous stomatitis in susceptible individuals or those with a hereditary predisposition to the disease. […] Hematinic (iron, folic acid, or vitamin B12) and zinc deficiencies have been demonstrated in some patients with recurrent aphthous stomatitis. […] HIV patients have reduced CD4 lymphocyte and elevated CD8 lymphocyte levels, predisposing them to RAS.

• #31 Mouth Ulcer: Causes, Symptoms, Diagnosis, and Treatment

  https://www.healthline.com/health/mouth-ulcers

  Mouth ulcers can also be a sign of conditions that are more serious and require medical treatment, such as: celiac disease, inflammatory bowel disease (IBD), including ulcerative colitis, diabetes, HIV, some autoimmune diseases, including: lupus, oral lichen planus, Behets disease, a rare condition that causes inflammation throughout the blood vessels.

• #32 Mouth ulcers: Types, causes, symptoms, and treatment

  https://www.medicalnewstoday.com/articles/317984

  Mouth ulcers are painful areas in the mouth and gums. […] While mostly harmless, mouth ulcers can be extremely uncomfortable and make it difficult for some people to eat, drink, and brush their teeth. […] In general, mouth ulcers are benign and harmless, although they can cause discomfort. Standard ulcers appear on the inner cheeks and last for about 1-2 weeks, and most clear up with no medical intervention. […] Experts do not fully understand why aphthous ulcers occur. However, some things may trigger a mouth ulcer, including: injury, such as biting the inner cheek or irritation from braces or dentures, stress, smoking, deficiencies in folic acid, iron, or vitamin B12, a weakened immune system, chemotherapy. […] Aphthous ulcers can be a symptom of systemic conditions, such as: Celiac disease, Crohns disease, Behcets disease, a rare autoimmune disorder, HIV and AIDS. […] Most mouth ulcers are harmless and heal on their own within 12 weeks, but larger or recurrent sores may require medical attention. […] Preventive measures include maintaining good oral hygiene, avoiding irritants like spicy foods, and addressing underlying health issues.

• #33 Recurrent Aphthous Stomatitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK431059/

  Recurrent aphthous stomatitis (RAS) is a chronic oral mucosa inflammatory disorder with an uncertain etiology. […] The etiology of recurrent aphthous stomatitis remains imperfectly understood. The cause is believed to be multifactorial, involving a cell-mediated immunological reaction and a genetic predisposition. Histopathological changes are seen before ulceration occurs. Lymphocytes (mononuclear cells) infiltrate the oral epithelium, edema develops, and the keratinocytes (oral epithelial cells) undergo vacuolization and vasculitis. This results in localized swelling and later ulceration of the epithelium. Infiltration with neutrophils, lymphocytes, and plasma cells occurs before the epithelium heals and regenerates. The pathogenesis of RAS is a T-cell-mediated immunological reaction involving the inflammatory cytokine named tumor necrosis factor-alpha (TNF-). TNF- activates the chemotaxis of neutrophils, generating an acute inflammatory response and the expression of the major histocompatibility (MHC) complex.

• #34

  https://journals.lww.com/apmd/fulltext/2017/14040/recurrent_aphthous_ulcers___still_a_challenging.3.aspx

  Recurrent aphthous ulcer (RAU) is a clinical condition characterized by painful ulcer with different size affecting the mucosa of the oral cavity. Its etiology and pathogenesis are not clearly known and the diagnosis is based on the clinical picture. […] The etiology of RAU remains unclear. Several etiological factors are thought to relate for causing this lesion such as trauma, immunological dysfunction, psychological stress, systemic diseases, nutritional deficiency, infections, and so on. […] Although the etiology of RAU is not clear, the defective immune regulation plays an important role. The Vitamin D has complex role in the regulation of immune system. The deficiency of Vitamin D is an important factor in etiopathogenesis of immune-mediated disorders. […] In RAU, the lesions develop over several days with different stages for forming aphthous ulcer. In the early phase, the patient will complain paresthesia before the development of the proper ulcer. First, a macula develops which progresses to a papule that later on becomes necrotic and ulcer formation.

• #35 Aphthous Stomatitis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1075570-overview

  Although the clinical characteristics of recurrent aphthous ulcer have been well defined, the precise etiology and the pathogenesis remain unclear. Many possibilities have been investigated. Recurrent aphthous ulcer is a multifactorial condition, and it is likely that immune-mediated destruction of the epithelium is the common factor in its pathogenesis. […] Immune dysregulation appears to play a significant role. Cytotoxic action of lymphocytes and monocytes on the oral epithelium may cause the ulceration, but the trigger remains unclear. Upon histologic analysis, recurrent aphthous ulcer consists of mucosal ulcerations with mixed inflammatory cell infiltrates. […] Researchers have disagreed about the role of microbes in the development of recurrent aphthous ulcers. The emphasis has been on a microbial agent as a primary pathogen or an antigenic stimulus. Numerous studies have failed to provide strong evidence to support the role of HSV, human herpesvirus (HHV), varicella-zoster virus (VZV), or cytomegalovirus (CMV) in the development of aphthous ulcers. […] Recurrent aphthous ulcer formation may be a T-cell-mediated response to antigens of Streptococcus sanguis that cross-react with the mitochondrial heat-shock proteins and induce damage to oral mucosa.

• #36 Recurrent Aphthous Stomatitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK431059/

  Recurrent aphthous stomatitis (RAS) is a chronic oral mucosa inflammatory disorder with an uncertain etiology. […] The etiology of recurrent aphthous stomatitis remains imperfectly understood. The cause is believed to be multifactorial, involving a cell-mediated immunological reaction and a genetic predisposition. Histopathological changes are seen before ulceration occurs. Lymphocytes (mononuclear cells) infiltrate the oral epithelium, edema develops, and the keratinocytes (oral epithelial cells) undergo vacuolization and vasculitis. This results in localized swelling and later ulceration of the epithelium. Infiltration with neutrophils, lymphocytes, and plasma cells occurs before the epithelium heals and regenerates. The pathogenesis of RAS is a T-cell-mediated immunological reaction involving the inflammatory cytokine named tumor necrosis factor-alpha (TNF-). TNF- activates the chemotaxis of neutrophils, generating an acute inflammatory response and the expression of the major histocompatibility (MHC) complex.

• #37 Aphthous Ulcers: Causes, Types, and Treatments

  https://ostrowonline.usc.edu/aphthous-ulcers-causes-types-treatments/

  Aphthous ulcers (oral aphthous), commonly known as canker sores, present a prevalent oral concern affecting 20-25% of the population. Oral apotheosis is a painful inflammatory process of the oral mucosa. The pathophysiology of oral aphthous ulcers remains unclear, but various bacteria are part of its microbiology (or cause the lesions to develop). Aphthous ulcers do not have a known cause, and an injury, stress, smoking, or deficiencies in folic acid, iron, or vitamin B12 may trigger this type of oral lesion. […] Recurrent aphthous stomatitis is a chronic inflammatory disease of the oral mucosa. It is characterized by painful mouth ulcers that an underlying disease cannot explain. […] Stressful life events are significantly associated with the onset of recurrent aphthous stomatitis (RAS) episodes, nearly tripling the odds of occurrence, highlighting the profound impact of psychosocial factors.

• #38

  https://www.aaaai.org/allergist-resources/ask-the-expert/answers/old-ask-the-experts/aphthous

  The results of this study suggest that certain SNPs of IL10 gene have association with predisposition of individuals to RAS. […] These findings confirm that mechanically induced injury of the oral mucosa may cause ulceration in people susceptible to aphthous stomatitis. […] Stressful life events were significantly associated with the onset of RAS episodes, but not with the duration of the RAS episodes. […] In patients with a history of RAS, stressful events may mediate changes involved in the initiation of new RAS episodes. Mental stressors are more strongly associated with RAS episodes than physical stressors.

• #39 Identification of the causal relationship between sleep quality, insomnia, and oral ulcers | BMC Oral Health | Full Text

  https://bmcoralhealth.biomedcentral.com/articles/10.1186/s12903-023-03417-w

  Our results revealed a negative genetic correlation between sleep duration and mouth ulcer (genetic correlation: -0.09, P=0.007), while a positive genetic correlation between insomnia and mouth ulcer was observed (genetic correlation: 0.18, P=2.51E-06). […] Furthermore, we demonstrated that longer sleep duration is significantly associated with a reduced risk of mouth ulcers (OR: 0.67, 95% CI: 0.540.83, P=2.84E-04), whereas insomnia is nominally associated with an increased risk of mouth ulcers (OR: 1.40, 95% CI: 1.011.95, P=0.044). […] This work provides robust evidence to support the notion that enhanced sleep quality may confer a decreased risk of oral ulcers, thereby bearing considerable clinical relevance. […] The potential association between sleep duration and oral diseases has been suggested in previous clinical and epidemiological studies, but the results have been inconsistent.

• #40 Identification of the causal relationship between sleep quality, insomnia, and oral ulcers | BMC Oral Health | Full Text

  https://bmcoralhealth.biomedcentral.com/articles/10.1186/s12903-023-03417-w

  Our results showed that higher sleep duration was significantly associated with a reduced risk of mouth ulcers, whereas insomnia was nominally associated with an increased risk of mouth ulcers. […] One possible reason is that sleep duration could affect mouth ulcers by modulating immunologic response and inflammatory mediators. […] It was suggested that sleep deprivation increased serum TNF-, IL-1, IL-6, IL-8, and MCP-1 levels, while excessive production of TNF-, IL-1, and IL-6 were associated with an increased risk of recurrent aphthous stomatitis. […] Therefore, inflammation and oxidative stress might be involved in the pathogenesis of how short sleep duration increased the risk of mouth ulcers. […] In summary, our study revealed that prolonged sleep duration was linked with a decreased risk of mouth ulcers, whereas insomnia was associated with an increased risk of mouth ulcers.

• #41 Aphthous stomatitis – Wikipedia

  https://en.wikipedia.org/wiki/Aphthous_stomatitis

  Evidence for the T cell-mediated mechanism of mucosal destruction is strong, but the exact triggers for this process are unknown and are thought to be multiple and varied from one person to the next. […] The thickness of the mucosa may be an important factor in aphthous stomatitis. […] The nutritional deficiencies associated with aphthous stomatitis (vitamin B12, folate, and iron) can all cause a decrease in the thickness of the oral mucosa (atrophy). […] Local trauma is also associated with aphthous stomatitis, and it is known that trauma can decrease the mucosal barrier. […] Hormonal factors are capable of altering the mucosal barrier. […] Various antigenic triggers have been implicated as a trigger, including L forms of streptococci, herpes simplex virus, varicella-zoster virus, adenovirus, and cytomegalovirus. […] Sodium lauryl sulphate (SLS), a detergent present in some brands of toothpaste and other oral healthcare products, may produce oral ulceration in some individuals.

• #42 Understanding Oral Ulcers: Pathophysiology, Causes, and Treatment Strategies | VITROBIO Medical Devices

  https://www.vitrobio.com/blog/scientific-news-1/understanding-oral-ulcers-pathophysiology-causes-and-treatment-strategies-24

  The pathophysiology of oral ulcers is a complex interplay of multiple factors. At its core, the process involves disruption to the mucosal integrity within the oral cavity. This disruption can be triggered by mechanical, chemical, hormonal, and infectious causes. Each cause leads to a cascade of cellular and molecular events, ultimately resulting in the characteristic ulcerative lesions. […] Mechanical trauma, for instance, often triggers oral ulcers through repetitive irritation or injury. Braces, sharp edges of teeth, ill-fitting dentures, or accidental biting can create minor wounds that develop into ulcers as the epithelial barrier is breached. […] Xerostomia or dry mouth enhances susceptibility to ulcers. Saliva serves multiple protective roles lubricating the mucous membrane, buffering pH, and controlling bacterial levels. With reduced saliva, the mucosal lining becomes more fragile and prone to trauma.

• #43 Understanding Oral Ulcers: Pathophysiology, Causes, and Treatment Strategies | VITROBIO Medical Devices

  https://www.vitrobio.com/blog/scientific-news-1/understanding-oral-ulcers-pathophysiology-causes-and-treatment-strategies-24

  Another key player in ulcer formation is epithelial atrophy, commonly seen post-radiotherapy. The thinning of the epithelial layer weakens the mucosal defense, making it easier for ulcers to form with minimal provocation. Inflammation of the mouth, known as stomatitis, is frequently accompanied by ulceration and represents an important early symptom. […] Infectious causes range from viral agents like herpes simplex and coxsackie A, to bacterial infections such as syphilis and tuberculosis. These pathogens invade the mucosal cells, eliciting an inflammatory response and cell-mediated immunity, which contribute to tissue destruction and ulceration. […] Chemical irritants, including certain ingredients in toothpaste like sodium lauryl sulfate (SLS), can also destabilize the mucosal layer. Prolonged exposure to these agents irritates the tissue, setting the stage for ulcer formation.

• #44 Integrating GWAS and proteome data to identify novel drug targets for MU | Scientific Reports

  https://www.nature.com/articles/s41598-023-37177-y

  Even with some efforts, the underlying mechanisms attributed to MU risk have remained elusive, making it difficult to translate identified risk loci into clinical interventions. […] By combining GWAS data with multidimensional QTL data, potential genes contributing to mouth ulcers will be identified. […] Ultimately, we identified 6 potential risk genes (BTN3A3, IL12B, BPI, FAM213A, PLXNB2, and IL22RA2) of mouth ulcers with altered protein abundances in the blood. Research into these genes may provide mechanistic and therapeutic targets. […] The expression of several butyrophilin (BTN) and butyrophilin-like (BTNL) molecules was significantly altered by inflammation, including BTN1A1, BTN2A2, BTN3A3, and BTNL8, and associated with tumor development. […] In conclusion, we found strong evidence supporting six novel blood proteins (BTN3A3, IL12B, BPI, FAM213A, PLXNB2, and IL22RA2) associated with mouth ulcers.

• #45 Integrating GWAS and proteome data to identify novel drug targets for MU | Scientific Reports

  https://www.nature.com/articles/s41598-023-37177-y

  Even with some efforts, the underlying mechanisms attributed to MU risk have remained elusive, making it difficult to translate identified risk loci into clinical interventions. […] By combining GWAS data with multidimensional QTL data, potential genes contributing to mouth ulcers will be identified. […] Ultimately, we identified 6 potential risk genes (BTN3A3, IL12B, BPI, FAM213A, PLXNB2, and IL22RA2) of mouth ulcers with altered protein abundances in the blood. Research into these genes may provide mechanistic and therapeutic targets. […] The expression of several butyrophilin (BTN) and butyrophilin-like (BTNL) molecules was significantly altered by inflammation, including BTN1A1, BTN2A2, BTN3A3, and BTNL8, and associated with tumor development. […] In conclusion, we found strong evidence supporting six novel blood proteins (BTN3A3, IL12B, BPI, FAM213A, PLXNB2, and IL22RA2) associated with mouth ulcers.

• #46 Aphthous Ulcers: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/867080-overview

  The elevated ratio supports an immunologic mechanism of disease and may have a diagnostic application in persons with RAS. […] A study by Zhang et al indicated that impairment of the enzymatic antioxidant defense system may be key to the pathogenesis of RAS in patients with the condition who have active lesions.

• #47 Genome wide analysis for mouth ulcers identifies associations at immune regulatory loci | Nature Communications

  https://www.nature.com/articles/s41467-019-08923-6

  The variants with larger effects on the odds of mouth ulcers are likely to be clinically informative. Many are located in or near genes or are enriched in pathways relating to T cell immunity, and tend to impose a Th1-type immune response, a biologically plausible mechanism that supports previous literature and resonates with clinical practice. […] Immune regulatory loci identified here may influence the susceptibility of infective or non-infective risk factors for mouth ulcers. A range of viral, bacterial and other changes in the oral microbiome have been suggested as acquired risk factors for mouth ulcers. It is possible that the genetic loci identified in this study relate to mouth ulcers through regulation of the host microbiome. […] One current view is that dysregulation of local cell-mediated response leads to an inappropriate focal accumulation of CD8+ T cell populations within the oral mucosa following minor triggers, leading to tissue damage and clinical manifestation as oral ulceration.

• #48 SciELO Brazil – Ulcerative lesions of the mouth: an update for the general medical practitioner Ulcerative lesions of the mouth: an update for the general medical practitioner

  https://www.scielo.br/j/clin/a/zRTxNQhZhJKwLc6RFT6xzXK/?lang=en

  Therapy for RAS is directed towards reducing the duration and/or frequency of episodes of ulceration. […] Lichen planus is by far the most common dermatological disorder that gives rise to oral ulcers. Lichen planus is an immunologically mediated disorder that is histopathologically characterized by an intense dermal infiltrate of T-lymphocytes. […] The precise trigger for this immunological reaction is unclear.

• #49 A New Hypothesis Describing the Pathogenesis of Oral Mucosal Injury Associated with the Mammalian Target of Rapamycin (mTOR) Inhibitors

  https://www.mdpi.com/2072-6694/16/1/68

  Topical steroids have been a mainstay in the treatment of inflammatory oral diseases such as aphthous and lichen planus. […] In particular, steroids (dexamethasone) effectively modulate the mTOR signaling pathway to interfere with the release of proinflammatory cytokines. […] The primary objective of this manuscript is to present some thoughts, based on what has been already reported, about the possible mechanisms by which mTOR inhibitors induce mucosal damage. […] The uniqueness of the oral cavity with respect to its inclusion of various forms of mucosa, multiple fluids (saliva, crevicular fluid), microflora, immune system (humoral, cellular and innate) and soft and hard tissue types provides a range of potential targets for side effects.

• #50 Management of Aphthous Ulcers | AAFP

  https://www.aafp.org/pubs/afp/issues/2000/0701/p149.html

  The pathophysiology of aphthous ulcers is poorly understood. Histologically, aphthae contain a mononuclear infiltrate with a fibrin coating. Patients with recurrent aphthae may have alteration of local cell-mediated immunity. Systemic T- and B-cell responses have also been reported as altered in patients with recurrent aphthae. […] The lack of clarity regarding etiology has resulted in treatments that are largely empiric and aimed at symptom reduction. […] Immune modulators used for the management of aphthous ulcers have been investigated most thoroughly in patients infected with HIV. Aphthous ulcers in HIV-infected patients may have extremely protracted healing times, up to months. Thalidomide (Thalomid) is the agent most frequently used for management of aphthous ulcers that cause severe pain with eating. Thalidomide in a dosage of 200 mg once to twice daily for three to eight weeks yields a faster healing rate than placebo.

• #51 Mouth ulcers: Types, causes, symptoms, and treatment

  https://www.medicalnewstoday.com/articles/317984

  Mouth ulcers are painful areas in the mouth and gums. […] While mostly harmless, mouth ulcers can be extremely uncomfortable and make it difficult for some people to eat, drink, and brush their teeth. […] In general, mouth ulcers are benign and harmless, although they can cause discomfort. Standard ulcers appear on the inner cheeks and last for about 1-2 weeks, and most clear up with no medical intervention. […] Experts do not fully understand why aphthous ulcers occur. However, some things may trigger a mouth ulcer, including: injury, such as biting the inner cheek or irritation from braces or dentures, stress, smoking, deficiencies in folic acid, iron, or vitamin B12, a weakened immune system, chemotherapy. […] Aphthous ulcers can be a symptom of systemic conditions, such as: Celiac disease, Crohns disease, Behcets disease, a rare autoimmune disorder, HIV and AIDS. […] Most mouth ulcers are harmless and heal on their own within 12 weeks, but larger or recurrent sores may require medical attention. […] Preventive measures include maintaining good oral hygiene, avoiding irritants like spicy foods, and addressing underlying health issues.

• #52 Mouth ulcers | Better Health Channel

  https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/mouth-ulcers

  If your oral health professional cannot determine the cause of your mouth ulcers, or if the ulcers do not respond to the normal treatments, you may need to have a biopsy of part of the ulcer and some of the surrounding tissue. A biopsy is a procedure where a tissue sample is taken for examination and diagnosis. […] Most mouth ulcers are usually harmless and resolve by themselves within 10 to 14 days. Other types of mouth ulcers, such as the aphthous variety or those caused by herpes simplex infection or skin rashes in the mouth need topical treatment (such as a mouthwash, ointment or gel). […] Its not possible to speed up the recovery of ulcers, but the symptoms can be managed, and the risk of complications reduced.

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