Common Oral Mouth Diseases Range From Simple To Complex
Have you ever wondered about the vast range of issues that can affect your mouth, from a simple canker sore to a life-altering systemic illness? The reality is that common oral diseases represent a wide spectrum of conditions, spanning from highly contagious viral infections to chronic, complex autoimmune disorders that impact the entire body.
Understanding the underlying causes (etiology), recognizing the subtle clinical manifestations, and knowing the appropriate management strategy is crucial for both early diagnosis and effective treatment.
In this deep-dive guide, we'll navigate the most significant conditions affecting the oral cavity and associated skin, including viral threats like Varicella Zoster Virus (VZV), autoimmune challenges such as Oral Lichen Planus (OLP) and Systemic Lupus Erythematosus (SLE), and various hypersensitivity reactions like Fixed Drug Eruptions. Get ready to empower yourself with the essential knowledge needed to identify and manage these conditions, ensuring long-term oral health and well-being.
Integrated Primary Keywords:
Common Oral Diseases
Oral Health
Autoimmune Disorders
Varicella Zoster Virus (VZV)
Oral Lichen Planus (OLP)
Systemic Lupus Erythematosus (SLE)
VARICELLA ZOSTER VIRUS (VZV) Chickenpox
Varicella zoster (VZV or known as human herpes virus with double-stranded DNA genome. VZV only infects humans with the main target is T lymphocytes epithelial cells and ganglia. Primary infection causes varicella (chickenpox), where VZV becomes latent in ganglionic neurons When cellular immunity to VZV decreases with age or in immunocompromised persons, active VZV returns to cause zoster (herpes zoster). Varicella zoster virus (VZV) is transmitted by droplets, aerosols and direct and responsible contact for varicella (chickenpox) and herpes zoster (HZ) .The former is a highly contagious, usually mild infection early in life Varicella in children usually resolves on its own although complications can be unpredictable and immune long-term follow-up after the patient recovers.
Varicella Chicken Pox (Chicken Pox)
Me is a disease caused by infection with Varicella Zoster Virus that attacks the skin and mucosa, and has a unique characteristic that is unilateral due to latent VZV reactivation
Clinical Manifestations on the skin
Prodermal symptoms Red, spots on the skin then become vesicles with lymphadenopathy, Starting from the upper part of the body then spreads to the area bottom In the oral cavity. Starting from the vesicles on the buccal mucosa, tongue, gums and palate. The vesicle lesion is surrounded by erythema.
Pathogenesis. After transmission to susceptible hosts VZV multiplies in the pharynx (tonsils), infects the T cells that enter the circulation and spreads the virus to the skin and possibly other organs. VZV can alter the shape of diverse T cell populations to facilitate skin trafficking. VZV DNA can be detected in T cells (viraemia) 10 days before the onset of the rash and can last for a week thereafter. Initially, innate immunity delays viral multiplication in the skin giving time for adaptive immunity to develop. Finally, the skin's innate immune response is overcome by the virus and there is substantial viral replication in the skin and occasionally viscera, resulting in a characteristic varicella rash.
Vvz enters via the upper respiratory tract and oropharynx.
Multiplication. Then follows blood and lymph flowPrimary viremia) Goes to the organs Reticulo Endothelial System (liver) Multiplication Follows blood flow (secondary viremia) To the skin and mucosa.
Clinical manifestations
Entematous papules Vesicles → Crusted crusts excreted Pustules → Rupture of excoriated crust from central (trunk, face) to the periphery ( limb). Walk following thesensory nerve fibers dorsalis Ganglion (Latent).
Behcet's Syndrome
Behcet's Syndrome syndrome is a chronic multisystem disease characterized by the "symptomatic triad" of recurrent oral cavity ulceration and genital ulcerations and eye lesions. This syndrome is also associated with other systemic manifestations such as the digestive system, central nervous system, and joint and vascular infections.
Etiology Immunocomplex that causes vasculitis of blood vessels and swelling of the epithelium. Genetic component factors in Dugn also play a role in the manifestation of this syndrome.
Symptoms
· Minor ulcers on the mucosa (first appeared on the palate of the lips of the tongue gingiva, oral mucosa and oropharynx
· The size of the lesion varies from 210 mm with a characteristic pseudomembranous covering the surface of the ulcer and critematous edges
· Genital ulcer (second lesion) male lesions occurs in the penis and scrotum of women occurs in the labia may labia minor vulva and walls vaginal with manifestations without pain that requires further clinical examination
· Eyes (conjunctivitis uveitis, renitis) occurs 2 3 years after onset.
· Characterized by blurred vision pain in the eye. uveitis , edema, optic atrophy or retinal conjunctivitis Accompanied i with headaches
Management & Treatment
Corticosteroid and immunosuppressant
Oral Lichen Planus (OLP)
chronic autoimmune amusal tiche found on the skin, oral mucosa, genital mucosa, scalp and nails with a higher incidence in women than men (2: 1).
Etiology not known, suspected hypersensitivity type 3, autoimmune. As a result of the abnormal T-cell-mediated immune response to basal pellets that are considered foreign bodies (T4 and T8 lymphocytes), causing surface changes. Predisposing or triggering factors include genetic, infectious and immunological factors.
Clinical Manifestations
· Pain when palpated
· Bilateral and wickham striae can occur on the buccal mucosa, tongue and lips.
· Reddish papules, lumped (oligonal), fused, to (itching → scratching crusting) often on the wrist
Classification
· Reticular (asymptomatic) Most common form of Wickham striae (Often buccal Asymetric and bilateral)
· Plaques (White solitaire lesions High incidence in gunshot smokers)
· Papular White lesions about 0.5-1.0 mm in diameter, small white papules with smooth striae on the margins
· Erythematous / atrophic , diffuse red lesion of white striae of the typeReticular surrounded by an erythematous area. Normally the gingiva,Continuation of the type atrophic thin layer of the epithelium has been abrasion ulceration & symptomatic lesions are often surrounded by keratin luminous striae.
· Erosion Bullous Showsblister whichin size increaseand and rupture> make the surface ulcerated Pain>Nikolsky sign may be positive.
Management & Treatment
· Corticosteroids-These are the main drugs used to treat OLP. This medicine can be used as a mouthwash, gel or ointment and can be applied directly to the affected area. The drug can also be injected directly or taken in pill form.
· Anesthesia-The use of painkillers or anesthetic mouthwashes can reduce the discomfort caused by the wound. This medicine should be used before meals.
· Preservatives-You can also use preservatives or gel mouthwashes. When the gums are painful and it is difficult to brush your teeth, this operation can prevent the accumulation of plaque.
· Steroid pills-These medications can also be used to relieve pain.
Mucous membrane pemphigoid (MMP)
mucous membranes are a group of chronic inflammatory autoimmune diseases. Subepithelial disease that predominantly affects the mucosa is characterized by membranes by linear deposition of IgG, IgA, or C3 along the lower epithelial membrane.
Etiology MMP is an autoimmune disorder with unknown etiology. Several predisposing factors such as inflammatory trauma to drugs (clonidine D penicillamine indomethacin). viral agents, UV rays and other autoimmune diseases.
Clinical Manifestations
MMP is a part of subepithelial bullous skin mucosal disorders that can occur with oral ocular lesions of the skin, genital nasopharynx, esophageal and larynx. In severe cases, m can cause blindness due to eye involvement and can even be life-threatening due to airway obstruction. It can affect any or all mucous membranes with or without the involvement of the skin in reducing the frequency of the oral cavity (90%), eyes (65%), nose. nasolarnyx anogenital dacrah of the skin (20-30%), larıng (8-9%). and the esophagus Most frequently present in MMP is desquamation of the gingiva and occurs frequently in postmenopausal women.
· Autoimmune reaction of membrane proteins Occurs in the gingiva, conjunctiva and rarely on the skin. General lesions in the mouth. Desquamative gingivitis.
· Persistent and painful.
· Patients older than 50 years.
Bullous Pemphigoid (BF)
Energy Bullous pemphigoid is an autoimmune blisters disease that predominantly affects the elderly. This immune-mediated disease is associated with humoral and cellular responses directed against two well-characterized antigens, namely the bullous pemphigoid antigen 1 MORNING) and bullous pemphigoid antigen (BPAG2) both components of the complex functional adhesion hemidesmosome in the skin and mucosa.
Clinical manifestations
· vesicles and bullae on the skin that appear
· normal or erythematous lesions are bullous not easily broken
· Attacking lamina lucidum and Inter epithelium and sub-epithelium
· often occur in elderly patients
Management & Treatment
· Chronic sub-epithelial blister blister due to autoantibody treatment Oral corticosteroids and analgesics can be given.
· Topical therapy includes Fluocinomide (0.05%) and clobetasol propionate (0.05%) used 3 times a day for 6 months moderate lesions.
· Triamcinolone acetonide 0.1%, flucinolone acetonide 0.05% clobetasol propionate 0.05% orabase 3-4 times a day used for 9-24 weeks → overcoming limited lesions
· Systemic therapy can be given including Prednisone 1-1.5 mg / kg / day by looking at the side effects of the drug.
Systemic Erythematous Lupus (SLE)
Systemic Tupus erythematosus (SLE) is a prototypic multisystem autoimmune disorder whose clinical presentation includes almost all organs and tissues, both skin and mucous membranes with or without systemic manifestation.
Etiology SLE is not known for sure but certain risk factors have been identified that cause immune system dysfunction with antibody formation and immune complex deposition. The predisposition for SLE is influenced by genetic factors that are predominantly female involving the contribution of certain hormones. Environmental factors such as smoking, exposure to ultraviolet light, viral infections and specific drugs (eg, sulfonamide antibiotics) are known to trigger SLE (Cunha et al 2016)
Pathogenesis SLE complex involves many components of the immune system With an underlying genetic predisposition to and in response to multiple triggers, the balance of the immune system shifts towards reacting to itself, instead of tolerance of T and B cells becoming activated, leading to antibody production and immune complex formation This complex circulates and settles in critical tissue causing organ injury.
Clinical Manifestations
· Butterfly rash In the skin
· erythematous rash
· Invadestissues the body'sand organs
· Ulceration of erythema and keratosis may be seen Often seen on vermilion, labial andmucosa of the
· buccalgingiva and palate. Early systemic symptoms mayfever,
· weight loss and malaise.
· include Systemic manifestations of arthritis pericarditis,disease
Management & Treatment.
basic recommendations including avoiding the sun and pe use high SPF sunscreen with screening and counseling for modifiable cardiovascular risk factors such as smoking Calcium and vitamin D supplements are recommended Anti-malarial drugs, hydroxychloroquine have been shown to be as beneficial as in treating mild lupus efficacy Administration of oral corticosteroids is considered a cornerstone treatment of SLE.
Lupus Erythematosus Discoid Disease
Lupus erythematosus can be seen in several forms, namely systemic lupus erythematosus (SLE), discoid lupus erythematosus (DLE) and sub-acute lupus. Lupus erythematosus is an autoimmune disease involving humoral and cell-mediated systems immune.
Predisposing factors
· Drugs
· Hormones
· viruses
· Genetic
· Sun exposure
Discoid Lupus Erithematous (DLE) Discord lupus crythematosus (DLE) is a chronic disease affecting the dermatome causing changes in scar tissue, hair loss and hyperpigmentation in the skin It has an effect on a person's quality of life, due to its chronic course. Prognosis can be improved if treatment is started as early as possible.
Etiology there are several conditions that cause lupus manifestations, such as genetics, environment and drugs. Partial deficiencies of complement C2 and C4 have been reported in chronic cutaneous lupus, including discoid lupus Genetic polymorphisms that cause this disease are pro-inflammatory cytokines, tyrosine kinase-2, Fc II receptor (FcRII), T cell receptor loci, adhest molecules, antioxidant enzymes, and Apoptotic genes Ultraviolet light can induce chronic cutaneous lupus and smoking is closely related to discoid lupus.
Clinical Manifestations
Oral discoid lesions are seen in 20% of patients. Without involvement of skin lesions or before skin lesions develop. oral lesions can be seen. The labial mucosa is most commonly affected at the vermillion border and the buccal mucosa. The occurrence of white papules, central erythema, irradiated white border zone of the striae and peripheral telangiectasia (small spots) is pathognomic.
Management & Treatment
· Excessive sun exposure, UV rays and heat are factors that trigger or exacerbate DLE Knim or sunscreen lotions for topical therapy applied regularly including ,fluocinolone, betamethasone, triamcinolone acetonide.
· Oral therapy may include: Oral prednisolone 0.5 mg / kg rapidly tapering over and 6 weeks.
· Hydroxychloroquine, initially 200 mg twice daily, reduced to 200 mg / day after response.
· Chloroquine sulfate 200 mg twice daily Tab auromyocin 6-9 mg / day.
Allergic Contact Cheillitis
Allergic contact cheilitis is one of the classified hypersensitivity types of allergies into type IV (slow) which occurs after mucosal contact with certain substances and 24 72 hours after exposure to the antigen of these substances, for example, drugs, cosmetics, metals, and other substances.
Etiology These allergens have small molecules (picric acid, dinitrochlorobenzene different herbal ingredients, cosmetics, some drugs, metals and other substances).
Symptoms
· Inflammation of the vermillion or surrounding skin can lower lip above or both and could involve the corners of the mouth
· In vermillion reddish dry desquamation and fissured
· burning sensation and itching, and in more severe conditions that can trigger vesicles and crusting Rarely involves the labial mucosa
· Patient complains of stiffness, itching, heat and pain on the lips • eczema-like lesions
Examination
Perform patch test → confirm diagnosis
Treatment & Management
· Eliminate the main causative factor Recognize symptoms, identify causes, recognize allergens and avoid
· Patients are prescribed non-steroidal anti-inflammatory drugs topical and multivitamins.
· Supportive therapy given contains vitamin C 750 mg and vitamin B12 12 mg.
Fixed Food Eruption (FFE)
Allergic reactions in the skin or mucocutaneous areas that occur with certain food allergies which are usually characterized by the occurrence of recurrent lesions at the same place and each consuming food that will increase the number of lesion sites.
Etiology Type IV hypersensitivity due to food Signs Symptoms. Fixed food eruptions usually appear as a solitary or a small amount of pruritic. limited erythematous macules that evolve into edematous plaques. These lesions usually leave hyperpigmentation at the site of the lesions.
Sign & Symtomps
Clinically persistent, non-migratory lesions are usually bluish-purple or brown gray macules on the skin. The lesions are usually seen 30 minutes to 48 hours.
Management & Treatment
· Eliminate the causative factors Corticosteroid drug aradinzin ex. Methyl Prednisolone.
· Administration of topical drugs.
Stomatitis Medicamentosa
Stomatitis Medicamentosa is a wide range of sensitivity reactions following the systemic intake of many drugs and chemicals in normal doses but not related to the pharmacological activity or toxicity of drugs.
Etiology Type I hypersensitivity reactions due to drugs being consumed.
Management & Treatment
• Elimination of causes
• Antihistamines (dipenhydramine, lorar Hidhe
• Corticosteroids
Oral Lichenoid Reaction (OLR)
Non-infectious, chronic relapsing inflammatory disease involving mucosal contact with allergens. Oral lichen planus (OLP) and oral lichen planus response (OLR) are clinically and histopathologically similar diseases. OLP is the result of T cell-mediated auto-inflammatory process against unknown antigens, while OLR may be caused by drugs, tooth restoration materials and dental plaque.
Etiology Hypersensitivity type IV with predisposing factors, namely drugs, contact with dental material (amalgam) but OLR patients with amalgam fillings near the lesion should be replaced, that is, a patch test should be performed when possible and when OLR is suspected to be caused by drugs.
Symptoms
• Asymmetric uniateral lesion
• Wickham striae present (white)
• Cannot be scrapped
• With or without erosive
• Usually on the tongue and buccal mucosa.
Examination
A biopsy or skin patch test can be done.
Treatment & Management
• Eliminate causative factors
• Oral rinse
Stomatitis Venenata
Stomatitis Venenata Who occur? idipatic? Etiology. Type IV hypersensitivity reaction due to contact with certain substances / objects. The most common preservatives and flavorings cause allergic reactions to the oral cavity.
Precipitating factors. Food, mouthwash, lipstick. toothpaste, metal materials (pegs), amalgam, printing materials, topical anesthetics and acrylics
Symptoms. In the acute condition, the complaint is burn sensation. The mucosal-oral appearance also varies from moderate to clear erythematous lesions with or without edema. In chronic conditions the affected mucosa may show erythema or white, hyperkeratotic lesions. (Angela et al, 2009)
• Swelling, ulceration, dry lips
• Lip feels thick
• Redness erytematus
Examination.
drug patch tests
Treatment & Management
• Eliminate the main causative factor (3K + 1 H) Recognize symptoms, identify causes, identify allergens and avoid
• Use corticosteroid drugs for the healing process.
Angiodema
Angiodema swelling of the skin, mucous membranes, or both, including the upper respiratory tract and digestive tract. which usually lasts from hours to 3 days, occurs more frequently in women than men.
Etiology Mediated by immunoglobulin E. allergens trigger a type 1 (rapid) hypersensitivity response in which activated mast cells release histamine and other vasoactive mediators. This is triggered by food or drugs.
Clinical Manifestations. Common sites of swelling include the periorbital, lips, tongue, pharynx and larynx. Swelling is usually asymmetrical and palpated soft. Swelling of the lips and eyes (periorbital) is the most common.
Treatment. Angiodema can develop rapidly, the first step taken is to check the airway whether it is closed or not, especially angiodema of the pharynx, larynx and tongue. Medication with Oral antihistamines and corticosteroids.
Herpangina
Herpangina is an acute infection caused by a coxsackievirus. type A4 characterized by the presence of ulcers on the posterior mole palate and oropharynx. The incubation period of this virus is 4-7 days and generally this viral infection affects children and usually occurs in the summer. The patient complained of sore throat and pain when used to swallow, then found lesions on the mole palate and oropharynx.
Etiology from food or drink that has been contaminated with patient feces (fecal-oral route) Through droplets of saliva that come out when a person coughs, sneezes, or talks.
Symptoms are preceded by several complaints in the form of: Fever (body heat between 30-40 degrees Celsius), malaise, pain in thrush lesions in the mouth of pineapple.
Symptoms arise after 3-5 days when the virus enters the patient's body.
 |
Clinical
Features Vesicles and ulcers on the posterior mole and palate, oropharynx, Pain swallowing V, Erythema, Sore throat.
Treatment
No special treatment is available, because herpangina is self-limiting disease.
Supportive therapy consists of maintaining proper hydration, control of fever, recommended administration of acetaminophen and giving antihistamines to help reduce pain
Fixed Drug Eruption (FDE)
Etiology Hypersensitivity type IV by (ciproflaxacin). Signs and Symptoms. FDE is usually due to drugs appearing solitary or a small amount of pruritic, limited macular. These lesions usually recur in the exact same place as each exposure to the causative drug, but after stopping drug administration they leave hyperpigmentation. Clinically persistent lesions are non-migratory and are usually gray, bluish-purple or brown macules on the skin. Lesions are usually seen 30 minutes to 8 hours after drug intake. A burning sensation often precedes the appearance of these lesions. FDE can occur anywhere on the skin or in the membrane of mucosa. The most commonly affected are the lips, palms, penis area, and groin. (Shiohara, 2009)
Mechanism FDEis a mechanism by which skin inflammation is caused by skin-resident T cells, a complex and multistep process that causes tissue damage. This damage occurs when intraepidermal CD8 + T cells are activated to directly kill keratinocytes and release large amounts of cytokines such as IFN [gamma] into the local microenvironment. Cytokines or nonspecific molecular-mediated adhesions from CD4 +, CD8 + T cells, and molecular-mediated neutrophils to specific tissues without recognizing their allied antigens will increase tissue damage, thus contributing to the later stages of development of FDE lesions. (Valdebrab et al, 2013).
Management Eliminate the causes of Fixed Drug Eruption (FDE) & Betamethason cream tube No. S. litt or on the lips
Writers: Dr. Robert Paschal Rajendra, B.DS., DDS and colleagues
