Stomatitis: Difference between revisions

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Different mechanism are understood to cause different types of stomatitis:<ref name="pmid15057287">{{cite journal| author=Sonis ST| title=The pathobiology of mucositis. | journal=Nat Rev Cancer | year= 2004 | volume= 4 | issue= 4 | pages= 277-84 | pmid=15057287 | doi=10.1038/nrc1318 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15057287  }} </ref>
Different mechanism are understood to cause different types of stomatitis:<ref name="pmid15057287">{{cite journal| author=Sonis ST| title=The pathobiology of mucositis. | journal=Nat Rev Cancer | year= 2004 | volume= 4 | issue= 4 | pages= 277-84 | pmid=15057287 | doi=10.1038/nrc1318 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15057287  }} </ref>


*Aphthous stomatitis:
*[[Aphthous stomatitis]]:
**It is the most common cause of oral ulcers. A definitive pathogenesis does not exist for aphthous stomatitis but the proposed mechanism involves immune system abnormalities and the presence of autoimmune antibodies. It is thought to be caused by some types of cytokine and T cell accumulation manifesting as a defective cell mediated arm of the immunity.Recurrence is very common in aphthous ulcers.<ref name="pmid8665304">{{cite journal| author=Ship JA| title=Recurrent aphthous stomatitis. An update. | journal=Oral Surg Oral Med Oral Pathol Oral Radiol Endod | year= 1996 | volume= 81 | issue= 2 | pages= 141-7 | pmid=8665304 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8665304  }} </ref><ref name="pmid17343257">{{cite journal| author=Dalghous AM, Freysdottir J, Fortune F| title=Expression of cytokines, chemokines, and chemokine receptors in oral ulcers of patients with Behcet's disease (BD) and recurrent aphthous stomatitis is Th1-associated, although Th2-association is also observed in patients with BD. | journal=Scand J Rheumatol | year= 2006 | volume= 35 | issue= 6 | pages= 472-5 | pmid=17343257 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17343257  }} </ref><ref name="pmid10668310">{{cite journal| author=Murray LN, Amedee RG| title=Recurrent aphthous stomatitis. | journal=J La State Med Soc | year= 2000 | volume= 152 | issue= 1 | pages= 10-4 | pmid=10668310 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10668310  }} </ref>
**It is the most common cause of oral ulcers. A definitive pathogenesis does not exist for aphthous stomatitis but the proposed mechanism involves immune system abnormalities and the presence of autoimmune antibodies. It is thought to be caused by some types of cytokine and T cell accumulation manifesting as a defective cell mediated arm of the immunity.Recurrence is very common in aphthous ulcers.<ref name="pmid8665304">{{cite journal| author=Ship JA| title=Recurrent aphthous stomatitis. An update. | journal=Oral Surg Oral Med Oral Pathol Oral Radiol Endod | year= 1996 | volume= 81 | issue= 2 | pages= 141-7 | pmid=8665304 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8665304  }} </ref><ref name="pmid17343257">{{cite journal| author=Dalghous AM, Freysdottir J, Fortune F| title=Expression of cytokines, chemokines, and chemokine receptors in oral ulcers of patients with Behcet's disease (BD) and recurrent aphthous stomatitis is Th1-associated, although Th2-association is also observed in patients with BD. | journal=Scand J Rheumatol | year= 2006 | volume= 35 | issue= 6 | pages= 472-5 | pmid=17343257 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17343257  }} </ref><ref name="pmid10668310">{{cite journal| author=Murray LN, Amedee RG| title=Recurrent aphthous stomatitis. | journal=J La State Med Soc | year= 2000 | volume= 152 | issue= 1 | pages= 10-4 | pmid=10668310 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10668310  }} </ref>
*Herpetic stomatitis:
*[[Herpetic stomatitis]]:
**This type is causes by [[HSV1]] virus. It is caused by the destructive effect cause by the virus on the tissues in the form of break down of the infected cells. The infection may start as vesicles that are typically pin-head like and ultimately rupture, resulting ulceration. As a characteristic to the virus these ulcers are painful, irregular in appearance and often have a yellow-grey covering layer.
**This type is causes by [[HSV1]] virus. It is caused by the destructive effect cause by the virus on the tissues in the form of break down of the infected cells. The infection may start as vesicles that are typically pin-head like and ultimately rupture, resulting ulceration. As a characteristic to the virus these ulcers are painful, irregular in appearance and often have a yellow-grey covering layer.
**After the lesions resolve, the virus travels though the nerves to the nerve cells and goes into a latent stage. It can then reactivate when the person becomes immunocompromised and cause symptoms.<ref name="pmid16451405">{{cite journal| author=Kolokotronis A, Doumas S| title=Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis. | journal=Clin Microbiol Infect | year= 2006 | volume= 12 | issue= 3 | pages= 202-11 | pmid=16451405 | doi=10.1111/j.1469-0691.2005.01336.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16451405  }} </ref>
**After the lesions resolve, the virus travels though the nerves to the nerve cells and goes into a latent stage. It can then reactivate when the person becomes immunocompromised and cause symptoms.<ref name="pmid16451405">{{cite journal| author=Kolokotronis A, Doumas S| title=Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis. | journal=Clin Microbiol Infect | year= 2006 | volume= 12 | issue= 3 | pages= 202-11 | pmid=16451405 | doi=10.1111/j.1469-0691.2005.01336.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16451405  }} </ref>
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*Chemotherapy associated stomatitis:
*Chemotherapy associated stomatitis:
**The Chemotherapy causes RNA and DNA damage by the reactive oxygen species leading to an excessive production of inflammatory cytokines. These cytosines cause inflammation thus causing breaks in the epithelium.
**The Chemotherapy causes RNA and DNA damage by the reactive oxygen species leading to an excessive production of inflammatory cytokines. These cytosines cause inflammation thus causing breaks in the epithelium.
*Denture stomatitis:
*[[Denture stomatitis]]:
**Denture stomatitis effects upto 67% of denture wearers. It moct commonly affects the palatal mucosa.<ref name="pmid3298586">{{cite journal| author=Arendorf TM, Walker DM| title=Denture stomatitis: a review. | journal=J Oral Rehabil | year= 1987 | volume= 14 | issue= 3 | pages= 217-27 | pmid=3298586 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3298586  }} </ref>The material used in fillings and dentures are porus because of the chemicals used and to give it a better grip. Pathogens like candida alibicans can colonize such suitable sites leading to an inflammatory response and thus denture stomatitis. The irritaitive effect of the foreign denture material can also contribute to the pathogenesis.<ref name="pmid28130176">{{cite journal| author=Abduljabbar T, Al-Askar M, Baig MK, AlSowygh ZH, Kellesarian SV, Vohra F| title=Efficacy of photodynamic therapy in the inactivation of oral fungal colonization among cigarette smokers and non-smokers with denture stomatitis. | journal=Photodiagnosis Photodyn Ther | year= 2017 | volume=  | issue=  | pages=  | pmid=28130176 | doi=10.1016/j.pdpdt.2017.01.182 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28130176  }} </ref><ref name="pmid25082257">{{cite journal| author=Marinoski J, Bokor-Bratić M, Čanković M| title=Is denture stomatitis always related with candida infection? A case control study. | journal=Med Glas (Zenica) | year= 2014 | volume= 11 | issue= 2 | pages= 379-84 | pmid=25082257 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25082257  }} </ref>
**Denture stomatitis effects upto 67% of denture wearers. It moct commonly affects the palatal mucosa.<ref name="pmid3298586">{{cite journal| author=Arendorf TM, Walker DM| title=Denture stomatitis: a review. | journal=J Oral Rehabil | year= 1987 | volume= 14 | issue= 3 | pages= 217-27 | pmid=3298586 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3298586  }} </ref>The material used in fillings and dentures are porus because of the chemicals used and to give it a better grip. Pathogens like candida alibicans can colonize such suitable sites leading to an inflammatory response and thus denture stomatitis. The irritaitive effect of the foreign denture material can also contribute to the pathogenesis.<ref name="pmid28130176">{{cite journal| author=Abduljabbar T, Al-Askar M, Baig MK, AlSowygh ZH, Kellesarian SV, Vohra F| title=Efficacy of photodynamic therapy in the inactivation of oral fungal colonization among cigarette smokers and non-smokers with denture stomatitis. | journal=Photodiagnosis Photodyn Ther | year= 2017 | volume=  | issue=  | pages=  | pmid=28130176 | doi=10.1016/j.pdpdt.2017.01.182 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28130176  }} </ref><ref name="pmid25082257">{{cite journal| author=Marinoski J, Bokor-Bratić M, Čanković M| title=Is denture stomatitis always related with candida infection? A case control study. | journal=Med Glas (Zenica) | year= 2014 | volume= 11 | issue= 2 | pages= 379-84 | pmid=25082257 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25082257  }} </ref>
*Noma or Gangrenous stomatitis:
*Noma or Gangrenous stomatitis:
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*[[Bovine papular stomatitis]]:
*[[Bovine papular stomatitis]]:
**[[Bovine papular stomatitis]] is a [[zoonotic]] disease. It is caused by [[bovine papular stomatitis virus]], starting as a single lesion and becoming a nodular mass ultimately. The virus has chemokine binding proteins that prevent the [[neutrophils]] and [[monocytes]] from migrating to the site of the pathology.<ref name="pmid27936239">{{cite journal| author=Sharif S, Nakatani Y, Wise L, Corbett M, Real NC, Stuart GS et al.| title=A Broad-Spectrum Chemokine-Binding Protein of Bovine Papular Stomatitis Virus Inhibits Neutrophil and Monocyte Infiltration in Inflammatory and Wound Models of Mouse Skin. | journal=PLoS One | year= 2016 | volume= 11 | issue= 12 | pages= e0168007 | pmid=27936239 | doi=10.1371/journal.pone.0168007 | pmc=5148066 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27936239  }} </ref><ref name="bovine papular stomatitis">{{cite book |last1=Mandell |firs1t=Gerald |last2=Gouglas |first2=Gordon |last3=Bennett |first3=John |date= |title=Principles and Practice of Infectious Diseases |location= Harvard Medical School |publisher=WILEY MEDICAL |page=988 |isbn=0-471-87643-7}}​</ref>
**[[Bovine papular stomatitis]] is a [[zoonotic]] disease. It is caused by [[bovine papular stomatitis virus]], starting as a single lesion and becoming a nodular mass ultimately. The virus has chemokine binding proteins that prevent the [[neutrophils]] and [[monocytes]] from migrating to the site of the pathology.<ref name="pmid27936239">{{cite journal| author=Sharif S, Nakatani Y, Wise L, Corbett M, Real NC, Stuart GS et al.| title=A Broad-Spectrum Chemokine-Binding Protein of Bovine Papular Stomatitis Virus Inhibits Neutrophil and Monocyte Infiltration in Inflammatory and Wound Models of Mouse Skin. | journal=PLoS One | year= 2016 | volume= 11 | issue= 12 | pages= e0168007 | pmid=27936239 | doi=10.1371/journal.pone.0168007 | pmc=5148066 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27936239  }} </ref><ref name="bovine papular stomatitis">{{cite book |last1=Mandell |firs1t=Gerald |last2=Gouglas |first2=Gordon |last3=Bennett |first3=John |date= |title=Principles and Practice of Infectious Diseases |location= Harvard Medical School |publisher=WILEY MEDICAL |page=988 |isbn=0-471-87643-7}}​</ref>
*Pyostomatitis vegetans:
*[[Pyostomatitis vegetans]]:
**Pyostomatitis vegetans is characterised by numerous painless, yellow, superficial pinpoint pustules with oedema of the mucosa of the mouth. It is found in patients with [[ulcerative colitis]]. The vesicles can combine and involve the [[vermillion border]] of the upper as well as the lower lips.<ref name="pmid28153136">{{cite journal| author=Magliocca KR, Fitzpatrick SG| title=Autoimmune Disease Manifestations in the Oral Cavity. | journal=Surg Pathol Clin | year= 2017 | volume= 10 | issue= 1 | pages= 57-88 | pmid=28153136 | doi=10.1016/j.path.2016.11.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28153136  }} </ref><ref name="pmid24713996">{{cite journal| author=Pellicer Z, Santiago JM, Rodriguez A, Alonso V, Antón R, Bosca MM| title=Management of cutaneous disorders related to inflammatory bowel disease. | journal=Ann Gastroenterol | year= 2012 | volume= 25 | issue= 1 | pages= 21-26 | pmid=24713996 | doi= | pmc=3959344 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24713996  }} </ref>
**Pyostomatitis vegetans is characterised by numerous painless, yellow, superficial pinpoint pustules with oedema of the mucosa of the mouth. It is found in patients with [[ulcerative colitis]]. The vesicles can combine and involve the [[vermillion border]] of the upper as well as the lower lips.<ref name="pmid28153136">{{cite journal| author=Magliocca KR, Fitzpatrick SG| title=Autoimmune Disease Manifestations in the Oral Cavity. | journal=Surg Pathol Clin | year= 2017 | volume= 10 | issue= 1 | pages= 57-88 | pmid=28153136 | doi=10.1016/j.path.2016.11.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28153136  }} </ref><ref name="pmid24713996">{{cite journal| author=Pellicer Z, Santiago JM, Rodriguez A, Alonso V, Antón R, Bosca MM| title=Management of cutaneous disorders related to inflammatory bowel disease. | journal=Ann Gastroenterol | year= 2012 | volume= 25 | issue= 1 | pages= 21-26 | pmid=24713996 | doi= | pmc=3959344 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24713996  }} </ref>
**The involvement of skin along with the oral mucosa is characterised by an entity called Pyodermatitis Pyostomatitis Vegetans.<ref name="pmid22068794">{{cite journal| author=Matias Fde A, Rosa DJ, Carvalho MT, Castañon MC| title=Pyodermatitis-pyostomatitis vegetans: case report and review of medical literature. | journal=An Bras Dermatol | year= 2011 | volume= 86 | issue= 4 Suppl 1 | pages= S137-40 | pmid=22068794 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22068794  }} </ref>
**The involvement of skin along with the oral mucosa is characterised by an entity called Pyodermatitis Pyostomatitis Vegetans.<ref name="pmid22068794">{{cite journal| author=Matias Fde A, Rosa DJ, Carvalho MT, Castañon MC| title=Pyodermatitis-pyostomatitis vegetans: case report and review of medical literature. | journal=An Bras Dermatol | year= 2011 | volume= 86 | issue= 4 Suppl 1 | pages= S137-40 | pmid=22068794 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22068794  }} </ref>

Revision as of 15:30, 6 March 2017

Stomatitis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]

Overview

Stomatitis is an inflammation of the mucous lining of any of the structures in the mouth, which may involve the cheeks, gums, tongue, lips, throat, and roof or floor of the mouth. Most physicians do not regularly examine the mouth of patients and so stomatitis or triggering conditions can remain undiagnosed unless they become symptomatic.[1] The inflammation of the structures in the mouth can be caused by a condition limited just to the mouth, such as poor oral hygiene, poorly fitted dentures, or from mouth burns from hot food or drinks, or by conditions that affect the entire body, such as medications, allergic reactions, or infections. A form of stomatitis known as stomatitis nicotina can be caused by smoking cigars, cigarettes, and pipes, and is characterized by small red bumps on the roof of the mouth.[2]

When it also involves an inflammation of the gingiva, it is called gingivostomatitis. Irritation and fissuring in the corners of the lips is termed angular stomatits or angular cheilitis. In children a frequent cause is repeated lip-licking and in adults it may be a sign of underlying iron deficiency anemia, or vitamin B deficiencis (e.g. B2-riboflavin, B9-folate or B12-cobalamins), which in turn may be evidence of poor diets or malnutrition (e.g. celiac disease).

Historical Perspective

  • Between 460-370 B.C., in relation to disorders of the mouth the term aphthae was first used by Hippocrates.[3]
  • In 1898, the first clinical description of the aphthous stomatitis was reported by Von Mikulicz and Kumme as a Mikuliez aphthea
  • In 1911, stomatitis aphthae recurrens cicatricicans was first described by Sutton.
  • In 1961, stomatitis aphthae recurrens herpetiformis was first described by Cooke.[4]

Classification

According to the etiology, stomatitis may be classified into:[5][6]

Infectious Stomatitis

  • Aphthous stomatitis
    • Major aphthous stomatitis
      • This type can last unto a few months and involves tonsils and the soft palate as well. It can subset for long intervals and then re appear.
    • Minor aphthous stomatitis
      • This is the characteristic form of aphthous stomatitis and is characterised by yellow-grey, painful minute ulcers in the anterior ora cavity in the buccal and oral mucosa with raised margins. They can last from a few days upto 2 weeks
    • Herpetiform stomatitis
      • These are multiple in number and effect the tongue at the lateral part and the tip. Ulcers are grey and very painful and are often accompanied by inability to eat. Intra nuclear inclusions can be found in the ulcers
  • Herpetic gingivostomatitis
  • Necrotizing ulcerative stomatitis or stomatitis gangrenosa(NOMA)[7]
  • Vesicular stomatitis
  • Vincent's stomatitis (Trench Mouth)
  • Enteroviral vesicular stomatitis with exanthem
  • Candida stomatitis

Other forms

  • Angular stomatitis
  • Denture stomatitis
  • Ulcerative or Chronic ulcerative stomatitis[8][9]
  • Contact stomatitis[10]
  • Migratory stomatitis or geographic stomatitis
  • Stomatitis nicotina
  • Pyostomatitis vegetans[11][12]
  • Bovine papular stomatitis[13]
  • Chemotherapy induced stomatitis

Pathophysiology

Different mechanism are understood to cause different types of stomatitis:[14]

  • Aphthous stomatitis:
    • It is the most common cause of oral ulcers. A definitive pathogenesis does not exist for aphthous stomatitis but the proposed mechanism involves immune system abnormalities and the presence of autoimmune antibodies. It is thought to be caused by some types of cytokine and T cell accumulation manifesting as a defective cell mediated arm of the immunity.Recurrence is very common in aphthous ulcers.[15][16][5]
  • Herpetic stomatitis:
    • This type is causes by HSV1 virus. It is caused by the destructive effect cause by the virus on the tissues in the form of break down of the infected cells. The infection may start as vesicles that are typically pin-head like and ultimately rupture, resulting ulceration. As a characteristic to the virus these ulcers are painful, irregular in appearance and often have a yellow-grey covering layer.
    • After the lesions resolve, the virus travels though the nerves to the nerve cells and goes into a latent stage. It can then reactivate when the person becomes immunocompromised and cause symptoms.[17]
    • Encephalitis associated with herpetic stomatitis is due to the interaction of HSV1 with Toll-like receptor 2 or TLR2
  • Chemotherapy associated stomatitis:
    • The Chemotherapy causes RNA and DNA damage by the reactive oxygen species leading to an excessive production of inflammatory cytokines. These cytosines cause inflammation thus causing breaks in the epithelium.
  • Denture stomatitis:
    • Denture stomatitis effects upto 67% of denture wearers. It moct commonly affects the palatal mucosa.[18]The material used in fillings and dentures are porus because of the chemicals used and to give it a better grip. Pathogens like candida alibicans can colonize such suitable sites leading to an inflammatory response and thus denture stomatitis. The irritaitive effect of the foreign denture material can also contribute to the pathogenesis.[19][20]
  • Noma or Gangrenous stomatitis:
    • Gangrenous stomatitis is also known as Noma or 'cancrum Doris'. Noma or gangrenous stomatitisIt is focal and destructive infection caused by Borrelia vincentii, Fusobacterium and Bacteroides. It is an acute infection of the tissues in the orofacial region. Immunocompromised individuals are predisposed to develop this condition. Noma or gangrenous stomatitis is more common in children. The infection can begin as a spot or vesicle on the gingival surface of the mandibular molars and premolars. This spot or vesicle is red initially and painful and develops into an ulcer. The lesion has cone shaped expansion with bone, teeth and tissue underneath being exposed after the soft tissue sloughs off.[6]
  • Bovine papular stomatitis:
  • Pyostomatitis vegetans:
    • Pyostomatitis vegetans is characterised by numerous painless, yellow, superficial pinpoint pustules with oedema of the mucosa of the mouth. It is found in patients with ulcerative colitis. The vesicles can combine and involve the vermillion border of the upper as well as the lower lips.[11][12]
    • The involvement of skin along with the oral mucosa is characterised by an entity called Pyodermatitis Pyostomatitis Vegetans.[23]

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

The common causes of stomatitis include:[17][24][14]

Gangrenous stomatitis

Following are a few causes of gangrenous stomatitis[6]

Bovine papular stomatitis

Causes by Organ System

Cardiovascular Kawasaki disease
Chemical/Poisoning Bismuthia, gold, mercury poisoning, nickel, thallium
Dental Angular cheilitis, angular stomatitis, aphthous stomatitis, aphthous ulcer, burning mouth syndrome, dentures, desquamative gingivitis, dry mouth, herpetic gingivostomatitis, hypertrophic gums, nicotine stomatitis, oral lesions, oral submucous fibrosis, oral ulceration, trench mouth, ulcerative gingivitis, Vincent's angina
Dermatologic Behcet's disease, bismuthia, erythema multiforme, gluten-sensitive enteropathy associated conditions, lip balm, pemphigoid, Stevens-Johnson syndrome, vesicular stomatitis with exanthem, warts
Drug Side Effect Acmella oleracea, afatinib, aflibercept, alemtuzumab, aminopterin, aralen phosphate, auranofin, benzydamine, bleomycin, boceprevir, busulfan, cabozantinib, capecitabine, carboplatin, cerubidine, chemotherapy, chloramphenicol, chloroquine phosphate, clofibrate, cosmegen, cyclophosphamide, cytosine arabinoside, dacarbazine, dactinomycin, daptomycin, daunorubicin, docetaxel, epirubicin,eribulin, etoposide, everolimus, floxuridine, fluorouracil, gemcitabine, gemtuzumab ozogamicin, gentamicin, ginkgo biloba, hexetidine, ixabepilone, ketorolac tromethamine, lenvatinib, levoleucovorin, lincomycin hydrochloride, lomustine, loratadine, melphalan, methotrexate, metronidazole, mitomycin, mitoxantrone, nabumetone, nicotine polacrilex, oxaliplatin, oxaprozin, oxcarbazepine, palbociclib, panitumumab, paraplatin, penicillin G potassium, pentostatin, peplomycin, pertuzumab, phenylbutazone, pixantrone, pralatrexate, pramipexole, procainamide, sargramostim, sirolimus, sodium aurothiomalate, sorafenib, sulfasalazine, sulindac, sunitinib, temsirolimus, thioguanine, tiagabine, tolmetin, trametinib, ziv-aflibercept
Ear Nose Throat Angular stomatitis, aphthous stomatitis, aphthous ulcer, glandular fever, oropharyngeal cancer, periodic fever, aphthous stomatitis, pharyngitis and adenitis, trench mouth, uvulitis, Vincent's angina
Endocrine Glucagonoma
Environmental No underlying causes
Gastroenterologic Celiac disease, Crohn's disease, dysphagia, inflammatory bowel disease, odynophagia, oropharyngeal candidiasis, ulcerative colitis
Genetic Chronic granulomatous disease
Hematologic Agranulocytosis, anemia, cyclic neutropenia, iron deficiency anemia, leukemia, neutropenia
Iatrogenic Irradiation
Infectious Disease Aphthous stomatitis, aphthous ulcer, arbovirus, baculovirus, bovine papular stomatitis, candidiasis, coxsackie virus, diphtheritic stomatitis, ebola, esophageal candidiasis, feline calicivirus, feline immunodeficiency virus, gangrenous stomatitis, glandular fever, hand-foot-and-mouth disease, herpangina, herpes simplex virus, herpes zoster, herpes, herpetic gingivostomatitis, HIV, infectious stomatitis, lassa fever, lichen planus, Marburg virus, noma (disease), oncolytic virus, oropharyngeal candidiasis, parapoxvirus, periodic fever, aphthous stomatitis, pharyngitis and adenitis, syphilis, trench mouth, tuberculosis, typhlitis, vesicular stomatitis virus, vesicular stomatitis with exanthem, vesiculovirus, Vincent's angina, warts
Musculoskeletal/Orthopedic Odynophagia
Neurologic Parkinson's disease
Nutritional/Metabolic Angular cheilitis, ariboflavinosis, folate deficiency, kwashiorkor, lingzhi, nutritional deficiency, pyrophosphate, vitamin B12 deficiency, vitamin B2 deficiency, vitamin B6 deficiency, vitamin C deficiency
Obstetric/Gynecologic Warts
Oncologic Cancer, glucagonoma, leukemia, oropharyngeal cancer
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric Emotional stress
Pulmonary No underlying causes
Renal/Electrolyte No underlying causes
Rheumatology/Immunology/Allergy Allergies, autoimmune diseases, Behcet's disease, chronic granulomatous disease, combined immunodeficiencies, drug hypersensitivity, gluten-sensitive enteropathy associated conditions, pemphigoid, periodic fever syndrome, systemic lupus erythematosus, TNF receptor associated periodic syndrome
Sexual No underlying causes
Trauma Trauma
Urologic No underlying causes
Miscellaneous Mucosa hemorrhage

Causes in Alphabetical Order[26] [27]

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3

Differentiating Stomatitis from other Diseases

Stomatitis should be differentiated from other disease as well as from possible underlying conditions causing stomatitis including:[6][28]

  • Tumors of the tongue
    • Squamous cell carcinoma
      • It can prevent as a non healing ulcer or as a mass and is mostly caused by smoking or alcohol utilization.[29]
    • Leukoplakia
      • It is benign but can progress to carcinoma after almost 10 years. It is common in atypical users of tobacco, other than smoking.[30]
      • Oral proliferative verrucous leukoplakia is an aggressive sub type that has multiple lesions and has higher conversion to warts or carcinoma.[31]
    • Melanoma
      • It has the typical abcde characteristics including asymmetry, irregular borders, color change, increase in diameter and evolution and is usually diagnosed in its later stages.[32]
    • Fordyce spots
      • These are benign neoplasms with sebaceous features
    • Torrus Paltinus
      • It is a nodular mass on the hard palate, covered with normal mucosa[33]
  • Autoimmune diseases
  • Agranulocytosis
  • Behcet's syndrome[16]
  • Nicorandil induced ulcers
      • It is a drug use in angina pectoris
  • Burning mouth syndrome
    • It is characterized by constant sensation of burning in the mouth in post menopausal women.
    • There is no particular cause for it and no specific treatment is done.
  • Syphilis
  • Coxsackie virus accompanies involvement of the hands and the mouth
  • HIV
  • VZV or Chicken pox

Epidemiology and Demographics

Age

  • Herpetic gingivostomatitis occurs mostly in children between 6 months to 5 years. It can also occur in other age groups.[17]
  • Noma or gangrenous stomatitis is more common in children[6]

Gender

  • Denture stomatitis is more common in females [18]

Season

  • Herpetic gingivostomatitis has no seasonal preference.[34]

Risk Factors

The following risk factors are believed to influence the development of stomatitis:[35][36]

Risk factors for denture stomatitis

Some risk factors for denture stomatitis include[18][20]

  • Poor denture hygiene
  • Overnight wearing of dentures
  • pH of oral mucosal surfaces < 6.5
  • Dietry deficiencies
  • Hematological diseases

Bovine papular stomatitis

  • Expoure to infected cow

Screening

Screening for stomatitis is not recommended.[38]

Natural History, Complications and Prognosis

Natural History

  • If left untreated herpetic stomatitis resolves after the vesicles erupt and the ulcers heal. The HSV travels length nerves and moves to the ganglions where it stays in latent form. When the host becomes immunocompromised after taking medications or due to some other illness, the virus assesses the opportunity and through the same nerves becomes active once again manifesting symptoms such as oral vesicles.[17]
    • The viral shedding can continue for 2-12 days after primary infection.[39]

Complications

Some complications of stomatitis include[17][40]

Life threatening complications

  • Meningoencephalitis

Other Common Complications

  • Recurrent skin and mouth infections
  • Dissemination of the infection

Noma Complications

  • Teeth loss

History and Symptoms

The diagnosis of stomatitis is mostly clinical. The location and features of the ulcers are also important findings in this regard. A detailed history followed by a physical exam is very helpful.[41][39]

History

Previous history of stomatitis is common among patients presenting with an episode. Some findings in the history are[17]

  • Bad breath
  • Refusal to drink or eat

General symptoms

Some general symptoms associated with herpetic stomatitis include[17]

HEENT

  • Painful swallowing
  • Neck pain

Physical Examination

A comprehensive physical exam has great significance in the diagnosis of stomatitis. The exam findings may include[17]

  • Oral pin-head vesicles
  • Oral mucosal ulcers
  • Submandibular lymphadenitis
  • Halitosis

Laboratory Findings

History and physical examination are the mainstay of diagnosing stomatitis. If required laboratory findings can play an important role in diagnosing and differentiating the particular type of stomatitis.

Herpetic Stomatitis

  • Viral culture
  • Tzank smear for active lesions
    • It can not differentiate between the various types of viruses that can cause stomatitis i.e HSV1, HSV2 or VZV
  • Serology
  • Studies using immunofluorescent techniques
  • PCR

Noma or Gangrenous stomatitis

The diagnosis of Noma or gangrenous stomatitis is made by:[6]

  • Culture of organisms
  • Biopsy showing deep tissue involvement

Medical Therapy

The therapy for stomatitis is governed by following principles:[42]

Denture stomatitis

  • In most cases correction of denture fitness, avoidance of plaque development and avoidance of continuous wearing of dentures helps correct the defect. Antiseptic and antifungal agents are not required in most cases.[18]

Herpetic stomatitis

Noma or Gangrenous stomatitis

Criteria for Hospitalization

The patient who develops the following conditions must be institutionalized[17]

  • Encephalitis
  • Epiglotittis
  • Pneumonitis
  • Immunocompromised status
  • Poor oral intake

Surgical Therapy

Noma or Gangrenous stomatitis

Surgery may be require in Noma in the following conditions[6]

  • Removal of the teeth that are loose
  • Surgery for cosmetic reasons

Primary Prevention

  • Adequate hydration
  • Oral hygiene
  • Denture hygiene
  • Prevention of exposure to bovine papular stomatitis virus infected cow

Secondary Prevention

References

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