Common Vesiculobullous Diseases Etiology,Clinical Presentation,Microscopic findings,Diagnosis,Differential diagnosis and Treatment

Epidermolysis Bullosa

Etiology

• A diverse group of predominantly cutaneous, but also mucosal, mechanobullous diseases

• Inherited form: autosomal dominant or recessive patterns may occur

• Acquired form (acquisita): autoimmune from autoantibodies (immunoglobulin G [IgG]) to type VII collagen deposited within the basement membrane zone and upper dermis or lamina propria

Clinical Presentation

• Variable, depending upon the specific form of many subtypes recognized

• Mucosal lesions range in severity from mild to debilitating, depending on subtype:

• Inherited forms have wide range of oral mucosal involvement, with most severe form (autosomal recessive, dermolytic) also demonstrating enamel hypoplasia and caries

• Acquisita form with mucous membrane pemphigoid variant shows oral and conjunctival erosions/blisters

• Mucosal involvement absent in several variants

• Scarring and stricture formation common in severe recessive forms

• Mucosa is often friable, but it may be severely blistered, eroded, or ulcerated.

• Loss of oral anatomic landmarks may follow severe scarring (eg, tongue mucosa may become smooth and atrophic with episodes of blistering and scarring).

• Obliteration of vestibules, reduction of oral opening, ankyloglossia

• Scarring can be associated with atrophy and leukoplakia, with increased risk for squamous cell carcinoma development.

Microscopic Findings

• Bullae vary in location depending upon the form that is present:

• Intraepithelial in nonscarring forms

• At epithelial–connective tissue junction in dystrophic forms

• Subepithelial/intradermal in scarring forms

• Ultrastructural findings are as follows:

• Intraepithelial forms associated with defective cytokeratin groups

• Junctional forms associated with defective anchoring filaments at hemidesmosomal sites (epithelial–connective tissue junction)

• Dermal types demonstrate anchoring fibril or collagen destruction.

Diagnosis

• Distribution of lesions

• Family history

• Microscopic evaluation

• Ultrastructural evaluation

• Immunohistochemical evaluation of basement membrane zone using specific labeled antibodies as markers for site of blister formation

Differential Diagnosis

• Varies with specific form

• Generally includes the following:

• Bullous pemphigoid

• Mucous membrane (cicatricial) pemphigoid

• Erosive lichen planus

• Dermatitis herpetiformis

• Porphyria cutanea tarda

• Erythema multiforme

• Bullous impetigo

• Kindler syndrome

• Ritter’s disease

Treatment

• Acquisita form:

• Some recent success with colchicine and dapsone

• Immunosuppressive agents including azathioprine, methotrexate, and cyclosporine may be effective

• Acquisita and inherited forms:

• Avoidance of trauma

• Dental prevention strategies including extra-soft brushes, daily topical fluoride applications, dietary counseling

Prognosis

• Widely variable depending on subtype

Erythema Multiforme

Etiology

• Many cases preceded by infection with herpes simplex; less often with Mycoplasma pneumoniae or other organisms

• May be related to drug consumption, including sulfonamides, other antibiotics, analgesics, phenolphthalein-containing laxatives, barbiturates

• Another trigger may be radiation therapy.

• Essentially an immunologically mediated reactive process, possibly related to circulating immune complexes

Clinical Presentation

• Acute onset of multiple, painful, shallow ulcers and erosions with irregular margins

• Early mucosal lesions are macular, erythematous, and occasionally bullous.

• May affect oral mucosa and skin synchronously or metachronously

• Lips most commonly affected with eroded, crusted, and hemorrhagic lesions (serosanguinous exudate) known as Stevens-Johnson syndrome when severe

• Predilection for young adults

• As many as one-half of oral cases have associated erythematous to bullous skin lesions.

• Target or iris skin lesions may be noted over extremities.

• Genital and ocular lesions may occur.

• Usually self-limiting; 2- to 4-week course

• Recurrence is common.

Diagnosis

• Appearance

• Rapid onset

• Multiple site involvement in one-half of cases

• Biopsy results often helpful, but not always diagnostic

Differential Diagnosis

• Viral infection, in particular, acute herpetic gingivostomatitis (Note: Erythema multiforme rarely affects the gingiva.)

• Pemphigus vulgaris

• Major aphthous ulcers

• Erosive lichen planus

• Mucous membrane (cicatricial) pemphigoid

Treatment

• Mild (minor) form: symptomatic/supportive treatment with adequate hydration, liquid diet, analgesics, topical corticosteroid agents

• Severe (major) form: systemic corticosteroids, parenteral fluid replacement, antipyretics

• If evidence of an antecedent viral infection or trigger exists, systemic antiviral drugs during the disease or as a prophylactic measure may help.

• See “Therapeutics” section for details.

Prognosis

• Generally excellent

• Recurrences common

 

Hand-Foot-and-Mouth Disease

Etiology

• A very common enterovirus infection (coxsackievirus A10 or A16), which may occur in mild epidemic proportion, chiefly in children

• Incubation period is short, usually less than 1 week

Clinical Presentation

• Oral mucosal lesions with focal herpes simplex–like appearance, usually involving nonkeratinized tissue (soft palate, floor of mouth, labial-buccal mucosa)

• Accompanying palmar, plantar, and digital lesions are deeply seated, vesicular, and erythematous

• Short course with mild symptoms

Diagnosis

• Concomitant oral and cutaneous lesions

• Skin lesions commonly involve hands and feet.

• Skin lesions may involve buttocks.

• Antibody-titer increase measured between acute and recovery phases

Differential Diagnosis

• Herpangina

• Herpes simplex infection

• Acute lymphonodular pharyngitis

Treatment

• Symptomatic treatment only

• Patient should be cautioned against the use of aspirin to manage fever.

Prognosis

• Excellent

• Lifelong immunity, but it is strain specific

Herpangina

Etiology

• Most often by members of coxsackievirus group A (7, 9, 10, and 16) or group B (1–5)

• Occasionally due to echovirus 9 or 17

Clinical Presentation

• Incubation period of 5 to 9 days

• Acute onset

• Usually endemic in young children; usually occurs in summer

• Often subclinical

• Posterior oral cavity, tonsillar pillars involved

• Macular erythematous areas precede short-lived vesicular eruption, followed by superficial ulceration

• Accompanied by pharyngitis, dysphagia, fever, malaise, headache, lymphadenitis, and vomiting

• Self-limiting course, usually under 2 weeks

Diagnosis

• Other viral illnesses to be ruled out or separated

• Course, time of year, location of lesions, contact with known infected individual

Differential Diagnosis

• Hand-foot-and-mouth disease

• Varicella

• Acute herpetic gingivostomatitis

Treatment

• Soft diet

• Hydration

• Antipyretics

• Chlorhexidine rinses

• Compounded mouth rinses

Prognosis

• Excellent

Herpetic Stomatitis: Primary

Etiology

• Herpes simplex virus (HSV)

• Over 95% of oral primary herpes due to HSV-1

• Physical contact is mode of transmission

Clinical Presentation

• 88% of population experience subclinical infection or mild transient symptoms

• Most cases occur in those between 0.5 and 5 years of age.

• Incubation period of up to 2 weeks

• Abrupt onset in those with low or absent antibody to HSV-1

• Fever, anorexia, lymphadenopathy, headache, in addition to oral ulcers

• Coalescing, grouped, pinhead-sized vesicles that ulcerate

• Ulcers show a yellow, fibrinous base with an erythematous halo

• Both keratinized and nonkeratinized mucosa affected

• Gingival tissue with edema, intense erythema, pain, and tenderness

• Lips, perioral skin may be involved

• 7- to 14-day course

Diagnosis

• Usually by clinical presentation and pattern of involvement

• Cytology preparation to demonstrate multinucleate virusinfected giant epithelial cells

• Biopsy results of intact macular area show intraepithelial vesicles or early virus-induced epithelial (cytopathic) changes

• Viral culture or polymerase chain reaction (PCR) examination of blister fluid or scraping from base of erosion

Differential Diagnosis

• Herpangina

• Hand-foot-and-mouth disease

• Varicella

• Herpes zoster (shingles)

• Erythema multiforme (typically no gingival lesions)

Treatment

• Soft diet and hydration

• Antipyretics (avoid aspirin)

• Chlorhexidine rinses

• Systemic antiviral agents (acyclovir, valacyclovir) if early in course or in immunocompromised patients

• Compounded mouth rinse

Prognosis

• Excellent in immunocompetent host

• Remission/latent phase in nearly all those affected who have adequate antibody titers

Impetigo

Etiology

• Cutaneous bacterial infection: Streptococcus and Staphylococcus species

• Is spread through direct contact

• Highly contagious

Clinical Presentation

• Honey-colored, perioral crusts preceded by vesicles

• Flaccid bullae less common (bullous impetigo)

Diagnosis

• Clinical features

• Culture of organism (usually group A, â-hemolytic streptococci or group II Staphylococcus aureus)

• Herpes simplex (recurrent)

• Exfoliative cheilitis

• Drug eruptions

• Other vesiculobullous diseases

Treatment

• Topical antibiotics (mupirocin, clindamycin)

• Systemic antibiotics

Prognosis

• Excellent

• Rarely, poststreptococcal glomerulonephritis may develop.

Mucous Membrane Pemphigoid

Etiology

• Autoimmune; trigger unknown

• Autoantibodies directed against basement membrane zone antigens

Clinical Presentation

• Vesicles and bullae (short lived) followed by ulceration

• Multiple intraoral sites (occasionally gingiva only)

• Usually in older adults

• 2:1 female predilection

• Ocular lesions noted in one-third of cases

• Proclivity for scarring in ocular, laryngeal, nasopharyngeal, and oropharyngeal tissues

Microscopic Findings        

• Subepithelial cleft formation

• Linear pattern IgG and complement 3 (C3) along basement membrane zone; less commonly IgA

• Direct immunofluorescence examination positive in 80% of cases

• Indirect immunofluorescence examination usually negative

• Immunoreactants deposited in lamina lucida in most patients

Diagnosis

• Biopsy

• Direct immunofluorescent examination

Differential Diagnosis

• Pemphigus vulgaris

• Erythema multiforme

• Erosive lichen planus

• Lupus erythematosus

• Epidermolysis bullosa acquisita

Treatment

• Topical corticosteroids

• Systemic prednisone, azathioprine, or cyclophosphamide

• Tetracycline/niacinamide

• Dapsone

• See “Therapeutics” section for details.

Prognosis

• Morbidity related to mucosal scarring (oropharyngeal, nasopharyngeal, laryngeal, ocular, genital)

• Management often difficult due to variable response to corticosteroids

• Management often requires multiple specialists working in concert (dental, dermatology, ophthalmology, otolaryngology)

Paraneoplastic Pemphigus

Etiology

• Autoimmune, triggered by malignant or benign tumors

• Autoantibodies directed against a variety of epidermal antigens including desmogleins 3 and 1, desmoplakins I and II, and other desmosomal antigens, as well as basement membrane zone antigens

Clinical Presentation

• Short-lived vesicles and bullae followed by erosion and ulceration; resembles oral pemphigus

• Multiple oral sites

• Severe hemorrhagic, crusted erosive cheilitis

• Painful lesions

• Cutaneous lesions are polymorphous; may resemble lichen planus, erythema multiforme, or bullous pemphigoid

• Underlying neoplasms such as non-Hodgkin’s lymphoma, leukemia, thymoma, spindle cell neoplasms, Waldenström’s macroglobulinemia, and Castleman’s disease

Microscopic Findings

• Suprabasilar acantholysis, keratinocyte necrosis, and vacuolar interface inflammation

• Direct immunofluorescent testing is positive for epithelial cell surface deposition of IgG and C3 and a lichenoid tissue reaction interface deposition pattern

• Indirect immunofluorescent testing is positive for epithelial cell surface IgG antibodies

• Special testing with mouse and rat bladder, cardiac muscle, and liver may demonstrate paraneoplastic pemphigus antibodies that bind to simple columnar and transitional epithelia

Diagnosis

• Biopsy of skin or mucosa

• Direct immunofluorescent examination of skin or mucosa

• Indirect immunofluorescent examination of sera including special substrates

Differential Diagnosis

• Pemphigus vulgaris

• Erythema multiforme

• Stevens-Johnson syndrome

• Mucous membrane (cicatricial) pemphigoid

• Erosive oral lichen planus

Treatment

• Identification of concurrent malignancy

• Immunosuppressive therapy

Prognosis

• Good with excision of benign neoplasms

• Grave, usually fatal, with malignancies

• Management is very challenging.

Pemphigus Vulgaris

Etiology

• An autoimmune disease where antibodies are directed toward the desmosome-related proteins desmoglein 3 or desmoglein 1

• A drug-induced form exists with less specificity in terms of immunologic features, clinical presentation, and histopathology

Clinical Presentation

• Over 50% of cases develop oral lesions as the initial manifestation

• Oral lesions develop in 70% of cases

• Painful, shallow irregular ulcers with friable adjacent mucosa

• Nonkeratinized sites (buccal, floor, ventral tongue) often are initial sites affected

• Lateral shearing force on uninvolved skin or mucosa can produce a surface slough or induce vesicle formation (Nikolsky sign)

Microscopic Findings

• Separation or clefting of suprabasal from basal layer of epithelium

• Intact basal layer of surface epithelium

• Vesicle forms at site of epithelial split

• Nonadherent spinous cells float in blister fluid (Tzanck cells)

• Direct immunofluorescence examination positive in all cases

• IgG localization to intercellular spaces of epithelium

• C3 localization to intercellular spaces in 80% of cases

• IgA localization to intercellular spaces in 30% of cases

• Indirect immunofluorescence examination positive in 80% of cases

• General correlation with severity of clinical disease

Diagnosis

• Clinical appearance

• Mucosal manifestations

• Direct/indirect immunofluorescent studies

Differential Diagnosis

• Mucous membrane (cicatricial) pemphigoid

• Erythema multiforme

• Erosive lichen planus

• Drug reaction

• Paraneoplastic pemphigus

Treatment

• Systemic immunosuppression

• Prednisone, azathioprine, mycophenolate mofetil, cyclophosphamide

• Plasmapheresis plus immunosuppression

• IVIg for some recalcitrant cases

• See “Therapeutics” section for details.

Prognosis

• Guarded

• Approximately a 5% mortality rate secondary to long-term systemic corticosteroid–related complications

Recurrent Herpetic Stomatitis: Secondary

Etiology

• Herpes simplex virus

• Reactivation of latent virus

Clinical Presentation

• Prodrome of tingling, burning, or pain at site of recurrence

• Multiple, grouped, fragile vesicles that ulcerate and coalesce

• Most common on vermilion border of lips or adjacent skin

• Intraoral recurrences characteristically on hard palate or attached gingiva (masticatory mucosa)

• In immunocompromised patients, lesions may occur in any oral site and are more severe (herpetic geometric glossitis).

Diagnosis

• Characteristic clinical presentation and history

• Viral culture or PCR examination of blister fluid or scraping from base of erosion

• Cytologic smear

• Direct immunofluorescence examination of smear

Differential Diagnosis

• Erythema multiforme

• Herpes zoster (shingles)

• Herpangina

• Hand-foot-and-mouth disease

Treatment

• Acyclovir or valacyclovir early in prodrome

• Supportive

• Acyclovir may be used for prophylaxis for seropositive transplant patients

• Ganciclovir may be used for human immunodeficiency virus (HIV)-positive patients, especially those co-infected with cytomegalovirus.

• For recurrent herpes labialis, see “Therapeutics” section.

Prognosis

• Excellent

• Healing without scarring within 10 to 14 days

• Protracted healing in HIV-positive patients

Stevens-Johnson Syndrome

Etiology

 • A complex mucocutaneous disease affecting two or more mucosal sites simultaneously

• Most common trigger: antecedent recurrent herpes simplex infection

• Infection with Mycoplasma also may serve as a trigger.

• Medications may serve as initiators in some cases.

• Sometimes referred to as “erythema multiforme major”

Clinical Presentation

• Labial vermilion and anterior portion of oral cavity usually affected initially

• Early phase is macular followed by erosion, sloughing, and painful ulceration

• Lip ulcers appear crusted and hemorrhagic.

• Pseudomembrane; foul-smelling presentation as bacterial colonization supervenes

• Posterior oral cavity and oropharyngeal involvement leads to odynophagia, sialorrhea, drooling

• Eye (conjunctival) involvement may occur.

• Genital involvement may occur.

• Cutaneous involvement may become bullous.

• Iris or target lesions are characteristic on skin.

Microscopic Findings

• Subepithelial separation with basal cell liquefaction

• Intraepithelial neutrophils

• Epithelial and connective tissue edema

• Perivascular lymphocytic infiltrate

Diagnosis

• Usually made on clinical grounds

• Histopathology is not diagnostic.

Differential Diagnosis

• Pemphigus vulgaris

• Paraneoplastic pemphigus

• Mucous membrane (cicatricial) pemphigoid

• Bullous pemphigoid

• Acute herpetic gingivostomatitis

• Stomatitis medicamentosa

Treatment

• Hydration and local symptomatic measures

• Topical compounded oral rinses

• Systemic corticosteroid use controversial

• Recurrent, virally associated cases may be reduced in frequency with use of daily, low-dose antiviral prophylactic therapy (acyclovir, famciclovir, valacyclovir).

• May require admission to hospital burn unit

Prognosis

• Good; self-limiting usually

• Recurrences not uncommon

Varicella and Herpes Zoster

Etiology

• Primary and recurrent forms due to varicella-zoster virus (VZV)

• Primary VZV (chickenpox): a childhood exanthem

• Secondary (recurrent) VZV (herpes zoster/shingles) infection: most common in elderly or immunocompromised adults

Clinical Presentation

• Varicella (chickenpox)

• Fever, headache, malaise, and pharyngitis with a 2-week

incubation

• Skin with widespread vesicular eruption

• Oral mucosa with short-lived vesicles that rupture forming shallow, defined ulcers

• Herpes zoster (shingles)

• Unilateral, dermatomal, grouped vesicular eruption of skin and/or oral mucosa

• Vesicles may coalesce prior to ulceration and crusting.

• Lesions are painful.

• Prodromal symptoms along affected dermatome may occur.

• Pain, paresthesia, burning, tingling

• Postherpetic pain may be severe.

Diagnosis

• Clinical appearance and symptoms

• Cytologic smear with cytopathic effect present (multinucleated giant cells)

• Viral culture or PCR examination of blister fluid or scraping from base of erosion

• Serologic evaluation of VZV antibody

• Biopsy with direct fluorescent examination using fluoresceinlabeled VZV antibody

Differential Diagnosis

• Primary herpes simplex/acute herpetic gingivostomatitis

• Recurrent intraoral herpes simplex

• Pemphigus vulgaris

• Mucous membrane (cicatricial) pemphigoid

Treatment

• Symptomatic management in primary infection

• Antiviral drugs (especially acyclovir) in immunocompromised patients or patients with extensive disease

• Systemic corticosteroids may be used to help control/prevent postherpetic neuralgia.

• Pain control to prevent “CNS imprinting”

Prognosis

• Generally good

• Recurrences more likely in immunosuppressed patients

The Temporomandibular System and Temporomandibular Disorders

Temporomandibular disorder or TMD is a broad term referring to problems with the jaws and their functioning. It is commonly referred to as "TMJ".This system is very complex and problems are caused by a variety of factors. This web page will attempt to give you a general overview of TMD so you can better understand the problems you may have been having.

The Temporomandibular System

The temporomandibular system consists of three basic components; the temporomandibular joint or TMJ, the teeth, and the neuromuscular system. 

Muscles of Mastication and TMJ

TMJ- This is the term often used to describe TMD, but it specifically refers to the joints that work your lower jaw, or mandible. These two joints are found just in front of the ears. Their close proximity to the ear is why some patients experience ear symptoms and can often hear the joint pop or crack. These two joints never act alone, that is, when your jaw functions, both joints will be working. There is a small cartilage disc between your lower jaw and skull in the joint. Some TMD problems are caused by dysfunction of this disk. When healthy it acts as a sort of "shock absorber" for the joint.

Teeth- The teeth are like the third leg of a tripod, the TMJ’s being the other two legs. The alignment of your bite and the functioning of the TMJ’s are intimately connected. Problems in any of the three areas may affect the other two.

Neuromuscular- This system is the nerves and muscles which work the temporomandibular system. It is important to realize that only the lower jaw, or mandible, moves during jaw function. The upper jaw, or maxilla, does not move; it is firmly attached to the skull. Therefore, the nerves and muscles are involved in moving the lower jaw only. The nerves transmit the messages for the muscles to move the jaw. They also transmit pain signals to the brain causing you to feel discomfort. The muscles are fairly large and are found from the side of your head down to your neck. Other related muscles that do not specifically work the jaw, but are sometimes symptomatic are found in the neck, face, and upper back.

What Defines TMD 

A wide spectrum of specific and non specific disorders that produce symptoms of pain and dysfunction of muscles of mastication,Temporomandibular joint and other associated structures.

Symptoms and signs of TMD can include some or all of the following.

Jaw pain and/or stiffness

Headaches, usually at the temples and side of head

Vague tooth soreness or toothaches which often move around the mouth

Sensitive teeth

Painful or tender jaw joint

Difficulty opening jaw

Pain and fatigue when eating hard or chewy foods

Clicks, pops, or grinding sound in jaw joint

Ear pain

Cervical neck tension and pain

Tooth wear

Diagnostic classification of Temporomandibular Disorders

Congenital or Developmental Disorders

• Aplasia 
• Hypoplasia 
• Hyperplasia 
• Neoplasia

Disc Dearrangement Disorders

• Disc displacement with reduction 
• Disc displacement without reduction

TMJ dislocation

Inflammatory disorders

• Capsulitis/Synovitis 
• Polyarthritides

Osteoarthritis

• Primary osteoarthritis 
• Secondary osteoarthritis

Masticatory Muscle disorders

• Myofacial Pain 
• Myositis 
• Myospasm 
• Myofibrotic  contracture 
• Neoplasia

Temporomandibular disorders come in many forms and varying degrees of severity. Basically TMD is a problem when you either experience pain and/or a loss of jaw function. The pain can range from a mild ache in the morning to a chronic debilitating pain. Loss of function can be mild jaw stiffness to being unable to open the jaw barely at all.

The symptoms of TMD can be an obvious jaw pain in the muscles near the mouth, but can also often exhibit as headache at the temples ("temporal headache"). This is due to inflammation in the large jaw closing temporalis muscle which is on either side of your head. To find this muscle place your hands on your temples and clench your teeth hard and you will feel this powerful muscle contract. Patients often feel this symptom is a tension headache or sinus headache but it can be easily differentiated during a TMD exam. Patients understandably (and many doctors) fail to make this connection between TMD and headaches.

The pain of TMD can come from either the muscles or the TM joint itself; often it comes from a combination of the two. The muscles can ache due to causes discussed below. Pain in the joint is usually due to inflammation within the structure itself. Sometimes the symptoms are found in other facial structures; such as dull ear pain, toothache, neck pain, etc. This referred pain is fairly common but it is important to rule out medical and/or dental causes of these pains prior to TMD treatment.

Loss of jaw function can be due to muscular and/or joint problems as well, just as pain can. The degree to which each is involved is determined through thorough history and exam.

Causes of TMD

Temporomandibular disorders rarely have a single cause. Any one of the following factors may contribute to TMD. Each patient presents with an individual combination of factors that are determined during history taking and clinical exam.

Trauma - Acute trauma to the jaws such as a car accident, a fall, a punch, etc. can cause damage to the muscles and/or joint. The acute pain and loss of function is usually responsive to conservative treatment. Sometimes trauma to the joint can cause chronic damage which may eventually contribute to a TMD problem at a later time.

Bruxism - Bruxism refers to a non functional grinding and clenching of the teeth. Some do this while awake but more often it is done while sleeping. Most people grind their teeth while sleeping to some degree. For whatever reason some people do this very hard to the point where they wear the enamel from their teeth. This bruxing is done by the jaw muscles and by the morning they can be painful due to fatigue. This constant pressure also can damage the TMJs over time. Bruxism is the most common factor found in TMD.

Malocclusion - This term means "bad bite". Sometimes when the teeth do not bite together in harmony with the shape and position of the joints it can place pressure on the joints. Missing teeth can sometimes contribute to this as well. The misalignment can also put strain on the jaw muscles. This factor can be mild to severe. Though the bite is an important part of the whole system it is only altered after conservative measures and only if it is felt improvement will result. In some patients discrepancies (known as interferences) become apparent after wearing the NTI device for a few months and a bite adjustment is recommended. Treatment of the bite for TMD is usually not needed but its contribution to the whole must be examined.

Emotion - Emotional stress often plays an integral role in the development of TMD. This occurs due to two basic reasons. Stress increases both the severity and duration of bruxism while asleep. Also, many will subconsciously clench and/or grind their teeth more while awake during times of stress. The other way stress contributes to TMD is that during times of stress your adaptability and pain threshold will go down. As a result you are more likely to experience symptoms of TMD if other factors already exist (bruxing, joint damage, etc.).

Emotional conditions beyond daily life stress can contribute to TMD as well. Depression, anxiety disorders, and the like can often have TMD problems arise. These conditions are quite stressful and it is not hard to imagine why TMD would develop.

Ergonomic - Your job and how you do it can contribute to TMD and related problems. If you work at a computer all day, for example, you may be holding your head in such a way that places strain on your TM system.

TMD Treatment

Treatment plans for TMD are as varied as the patients that present with it. Each patient must be treated differently depending on the uniqueness of their problems and the contributing factors. Pain Relief Info.

It is very important to realize that the goal of TMD treatment is to minimize pain and establish a return to function. TMD conditions are not "cured" but are managed instead. The basic goal is to allow the muscles and joints to heal through rest and care. Often damage to the joint itself can not be reversed, but the body can often heal it enough to return to function without pain. We also want to teach you to recognize the symptoms early and manage them yourself once we give you the tools to do so. This condition can often recur later on but early care can minimize the severity.

The basic philosophy of treatment is to do the conservative and reversible treatments first. Irreversible treatments, such as surgery or orthodontics, are only considered if conservative steps have failed to bring lasting relief. These more radical treatments are rarely used. Most patients respond well to simpler care.

The following treatment modalities may be used in each case.

Conservative treatment

• Patient education and self care 
• Rest and relaxation 
• Cognitive behavioral intervention 
• Pharmacotherapy 
• Occlusal therapy 
• Occlusal therapy 
• Orthopedic appliances 
• Physiotherapy 
• Rehabilitation of Denatal deficits 
• Management of trigger points

Surgical Treatment

• Arthrocentesis 
• Arthroscopy 
• Arthroplasty 
• Discectomy 
• Condylectomy

Occlusal Splint - Also called a night guard is designed to protect the teeth from further wear. These also will reduce the severity of grinding at night and allow the muscles to rest. In more severe cases it needs to be worn all day as well to allow the TMJ and muscles to rest.