Oral Manifestations of Autoimmune Blistering Diseases

[drsushant]

Background

Background
Oral lesions are observed commonly in autoimmune blistering skin diseases. Oral lesions can be the predominant or minor clinical manifestation of a given disease. Pemphigus vulgaris and bullous pemphigoid are the earliest recognized autoimmune blistering diseases, and, together, they account for about one half of the autoimmune blistering diseases. While most patients with pemphigus vulgaris have oral lesions, only a few patients with bullous pemphigoid have oral lesions. Over the last few decades, many other autoimmune blistering diseases have been delineated, and some of these newly identified diseases have oral manifestations.

This article discusses the oral manifestations of several well-characterized autoimmune blistering diseases, including pemphigus vulgaris, bullous pemphigoid, linear immunoglobulin A (IgA) bullous dermatosis, and paraneoplastic pemphigus. A group of autoimmune blistering diseases affecting primarily the mucous membrane is termed cicatricial pemphigoid or mucous membrane pemphigoid.

Pemphigus group
Pemphigus vulgaris is a very rare acantholytic skin disease. In most cases, oral involvement is severe, and the mouth sometimes can be the first site to exhibit lesions. Flaccid vesicles on the gums, tongue, and palate evolve rapidly into erosions and ulcerations with indistinct margins and peripheral sloughing of mucosal epithelium (Nikolsky sign). Pemphigus foliaceus, the most common form of pemphigus observed in animals, affects dogs and cats. It usually does not affect oral and other mucosal membranes.

Pemphigoid group
Bullous pemphigoid

In dogs and cats with bullous pemphigoid, oral involvement is seen in less than 50% of them. When present, mucosal lesions consist of vesicles and sharp-edged erosions and ulcers of the gum. In horses with bullous pemphigoid, mucosal sloughing appears early, and oral ulceration is widespread and severe. By contrast, pigs with bullous pemphigoid do not exhibit oral lesions.

Mucous membrane pemphigoid

Dogs and cats with the recently recognized mucous membrane pemphigoid exhibit lesions that predominate at mucosae and mucocutaneous junctions. Tense oral vesicles can occur early in the course of the disease. However, at the time of diagnosis, most animals present with mild-to-severe oral erosions and ulcerations. These lesions occur most commonly on the gum but also occur on the tongue and palate. Lesions occasionally extend to the lips. German shepherd dogs comprise approximately one third of the animals with mucous membrane pemphigoid.

Linear IgA bullous dermatosis

Oral lesions were present in 2 dogs with this disease, albeit being of minimum severity.

Epidermolysis bullosa acquisita

This disease can be divided into 2 forms. The generalized inflammatory form (seen most commonly in Great Dane dogs) is associated with rapid and extremely severe sloughing of the oral mucosa. The severe oral lesion is associated with anorexia and weight loss and can lead to sepsis. No oral lesions were observed in 1 dog with the localized form.

Bullous systemic lupus erythematosus

Ulceration of both the tongue and lips was observed in 1 dog with bullous systemic lupus erythematosus.

Paraneoplastic pemphigus
The association with thymic lymphosarcoma was documented in the only dog reported to have paraneoplastic pemphigus. Oral lesions in this dog were severe, consisting of mucosal erosions and ulcerations

        

[drsushant]

 images..

        

[drsushant]

Pathophysiology
As a group, autoimmune blistering skin diseases are recognized as autoantibody-mediated diseases. This group of diseases can be divided into 2 major subsets, the pemphigus subset and the pemphigoid subset. Whereas the pemphigus subset of diseases is mediated by autoantibodies that target the extracellular skin components that link one epidermal cell to another, the pemphigoid subset of diseases is mediated by autoantibodies that target the extracellular skin components that link the skin basement membrane components either to the lowermost layer of epidermal cells or to the dermal components. Accordingly, the pemphigus subset of diseases is termed intraepidermal blistering disease, while the pemphigoid subset of diseases is named subepidermal blistering disease. Passive transfer experiments have demonstrated that purified autoantibodies from patients with the pemphigus group of diseases can induce blister formation when delivered to newborn mice.

Passive transfer experiments using autoantibodies from human patients with 2 major forms of the pemphigoid group of diseases (ie, bullous pemphigoid, epidermolysis bullosa acquisita) failed to induce clinically observable blisters in newborn mice; however, rabbit antibodies raised against the recombinant proteins encoded by the gene of mouse bullous pemphigoid antigen 2 (BP180) are capable of inducing blisters in newborn mice in a complement-dependent manner. Furthermore, anti-BP180 autoantibodies from patients affected with BP are capable of inducing dermal-epidermal separation in cryosections of normal human skin, further supporting the pathogenic role of BP180.

In addition, rabbit antibodies raised against type VII collagen (epidermolysis bullosa acquisita antigen) are also capable of inducing blisters in mice. So far, no truly active experimental animal models (in which healthy mice are induced to autoimmune disease de novo) are known to facilitate the studies on the induction phase of autoimmune blistering diseases. Nevertheless, autoantibodies can be induced by immunized healthy BALB/c mice with synthetic peptides of the mouse bullous pemphigoid antigen 2 NC16A domain.

In certain patient subsets, the development of the autoimmune disease has been proposed to have been triggered by an immune phenomenon, “epitope spreading,” a concept stating that tissue injuries from an inflammatory event may expose the previously hidden autoantigen to autoreactive lymphocytes, leading to autoimmune disease. Possible clinical examples include mucous membrane pemphigoid and paraneoplastic pemphigus. For example, patients who developed ocular mucosal injury secondary to an inflammatory disease termed Stevens-Johnson syndrome are noted to subsequently develop ocular mucous membrane pemphigoid.

        

[drsushant]

History
Autoimmune blistering skin diseases generally have an insidious onset. The following may be noted on history:

When oral lesions are present, they invariably are symptomatic, varying from mild to unbearable pain.
Patients with mucous membrane pemphigoid often complain of spontaneous gum bleeding.
Lesions start to surface in the oral cavity by approximately 6 months prior to the skin lesions in most patients with pemphigus vulgaris.
In some patients who have oral manifestations of autoimmune blistering diseases, the symptoms are so severe that they prevent them from proper dietary intake, resulting in severe malnutrition.
In patients who have rectal involvement, pain and bleeding could be early symptoms.
In patients with laryngeal involvement, hoarseness could be an early symptom.
Intractable hemorrhagic stomatitis is highly suggestive of paraneoplastic pemphigus.

Physical
Oral manifestations of autoimmune blistering diseases generally can affect any area of the oral cavity, including the gingiva, palate, buccal, tongue, floor of the mouth, and pharynx. In the pemphigus disease group, the blisters are broken easily; therefore, they rarely are observed clinically. Instead, erosions and superficial ulcers more likely are observed. In the pemphigoid disease group, because the blisters are situated deeply, they are more likely to be observed intact clinically. Note the following:

In pemphigus vulgaris, oral lesions occur in most patients. In most patients, the oral mucous membranes are affected within 6 months of disease onset. In some patients, it remains exclusively an oral disease for months or years before generalized skin disease develops. Typically, small blisters rapidly evolve into erosions covered with white-yellow pseudomembranes. All areas of oral mucous membranes, gingiva, buccal, palate, tongue, and floor of the mouth can be affected (see the image below). A subgroup of patients with pemphigus vulgaris does not develop skin disease.
Oral manifestations, including blisters, hemorrhagic erosions, and crusts, are shown on a patient with pemphigus vulgaris.
Pemphigus foliaceus is predominantly a skin disease. Oral or other mucous membrane involvements are very rare. In skin, desmoglein-3 is present predominantly in the lower layers of epithelial cells. By contrast, the layers of desmoglein-3 are present throughout the upper and lower layers of epithelium in the oral mucous membrane. Thus, the autoantibodies of patients with pemphigus foliaceus, which exclusively target desmoglein-1, are unable to break down the adherence of the upper layers of epithelium of oral mucosa, which is protected by the presence of desmoglein-3.
In paraneoplastic pemphigus, oral lesions, which are invariably present in this disease, can precede, follow, or appear at the same time of neoplasm discovery. Severe mucositis with hemorrhagic blisters, erosion, or ulceration can be observed in various oral mucosae. Lesions at the vermilion border almost always are present.
In patients with bullous pemphigoid, oral lesions rarely are observed. If present, they usually are mild and consist of small blisters or erosions. In one patient with bullous pemphigoid and hemophilia, extensive bullous lesions occurred in the mouth, along with substantial bleeding.
In the rare occurrence of lichen planus pemphigoides, small blisters and flat, linear, white, netlike striae that characterize lichen planus can occur in oral mucous membranes.
With linear IgA bullous dermatosis (of adult and children), the oral lesions, rarely present, are similar to that of bullous pemphigoid or can mimic aphthaelike ulcers.
Oral lesions in epidermolysis bullosa acquisita commonly are observed. The lesions are deep-seated blisters, erosions, and ulcers, sometimes hemorrhagic. Milia are clinically observed.
Regarding mucous membrane pemphigoid, the oral mucous membrane is the most frequently affected site in this heterogeneous group of diseases, followed by ocular, skin, nasal, genital, pharyngeal, esophageal, laryngeal, and anal mucous membranes. Approximately 50% of patients with mucous membrane pemphigoid have oral mucosal lesions, as shown in the image below.

        

[drsushant]

images..

        

[drsushant]

 images..

        

[drmithila]

Causes
Autoimmune blistering diseases generally are caused by autoantibodies targeting the skin components of the epithelial cell surfaces or basement membrane zone. Certain human leukocyte antigen (HLA) alleles have been reported to be associated with autoimmune blistering diseases. For example, HLA-DQB1*0301 is associated strongly with bullous pemphigoid and mucous membrane pemphigoid.

Pemphigus group
Desmoglein-3 is the primary target antigen in pemphigus vulgaris, and desmoglein-1 is the exclusive target antigen in pemphigus foliaceus. In passive transfer experiments, these autoantibodies apparently induced (in newborn mice) blisters that have similar histology as the human diseases. These autoantibodies apparently are capable of inducing the blisters without the help of complement components; however, autoantibodies against desmoglein-1 are present in patients with pemphigus vulgaris and are capable of inducing blisters in newborn mice.

Paraneoplastic pemphigus
No true cause has been firmly established. Some patients have autoantibodies against desmoglein-3, and these autoantibodies can induce blisters in newborn mice. The possible link between the underlying neoplasm and autoimmunity may be due to an immune dysregulation secondary to the presence of neoplasm. In addition to autoantibodies to desmoglein-3, most patients develop autoantibodies to many intracellular epithelial components, desmoplakins I and II, periplakin, envoplakin, BP230 (BPAg1), and a 170-kd membrane protein. Several other smaller proteins are involved.

Autoantibodies to these intracellular components probably develop as a secondary autoimmune response rather than a primary cause. Neoplasms are clearly associated with paraneoplastic pemphigus. The most common associated benign tumor is thymoma, followed by Castleman tumor, a rare and complex lymphoproliferative disease. The most common associated malignant tumor is non-Hodgkin lymphoma, followed by chronic lymphocytic leukemia.

Pemphigoid group
Autoantibodies to BP180 are the likely inducing autoantigen. Passive transfer experiments using rabbit antimouse BP180 antibodies induce blisters in newborn mice, and the blister induction apparently is complement dependent. The target antigen for linear IgA bullous dermatosis (childhood and adult) is a truncated BP180 protein. The target antigen for epidermolysis bullosa acquisita is type VII collagen, particularly the noncollagenous (NC1) domain.

Mucous membrane pemphigoid
Multiple target antigens have been identified, including BP180, laminin-5, laminin-6, type VII collagen, and beta-4 integrin, but no clinical hallmark distinguishes subsets of patients with regard to the target antigen. Rabbit antibodies generated against laminin-5 can induce blisters in newborn mice. Presently, the link between the autoantibodies and the scarring process that characterizes this group of diseases is missing.

        

[drmithila]

Differentials

Aphthous Stomatitis
Behcet Disease
Erythema Multiforme
Herpes Simplex
Herpes Zoster
Lichen Planus
Oral Lichen Planus
Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

Medical Care
Patients with oral manifestations of autoimmune blistering diseases can be treated conjointly with an oral medicine specialist. Furthermore, patients should have an oral prophylaxis performed by a dental hygienist or dentist prior to initiation of systemic or topical therapy. During the course of therapy, patients should have oral prophylaxis (oral hygiene) performed every 3-4 months. Additionally, they should be monitored for oral candidiasis, especially once on immunosuppressive therapy.

For patients who are treated with systemic corticosteroid, daily calcium and vitamin D supplements are needed to reduce steroid-induced osteoporosis.

For patients who are treated with systemic corticosteroids, steroid-induced osteoporosis should be prevented or reduced by taking an osteoclast-mediated bone resorption inhibitor-bisphosphonate (eg, Fosamax).[18, 19]

For patients who have not responded to more conventional therapies, intravenous infusion of humanized monoclonal antibodies to B cells (anti-CD20, rituximab) could be used, after the precaution to assess for serious infections is taken into account.[20, 21, 22, 23]

Surgical Care
Surgical care usually is not needed in treating the oral manifestations of patients with autoimmune blistering diseases.

Consultations
Examination by pulmonary specialists is recommended for patients with severe oral lesions, especially those patients with paraneoplastic pemphigus if the patients have symptoms or signs suggestive of respiratory difficulty. Respiratory failure and death have been reported in these patients.[24, 25]

Examination by gastroenterologists is recommended for some patients with severe oral lesions to detect possible involvement of the esophagus. Dysphagia can be an associated symptom.

Examination by ophthalmologists experienced in external eye diseases is recommended for those patients with oral lesions and symptoms or signs of ocular inflammation.

Thorough examination by consulting physicians experienced in mucous membrane pemphigoid (cicatricial pemphigoid) is recommended for some patients with oral lesions that also can have genital mucosal involvement.

Care provided by oral medicine specialists or physicians experienced in the field of oral medicine is recommended for patients with severe oral disease.

Diet
Advise patients with oral mucosal manifestations of autoimmune blistering diseases to eat a balanced diet and to avoid rough or spicy foods. Patients generally have no dietary restrictions once the disease is under control.

During periods of flare-up, soft and bland diets are preferred since it will cause less trauma to the injured tissue. Foods with strong acidity and spicy foods should be avoided. Patients with epidermolysis bullosa acquisita should avoid foods with a hard-to-chew quality since this disease tends to be exacerbated by minor trauma.

Activity
Generally, no activity restrictions are recommended for patients with oral manifestations of autoimmune blistering diseases; however, strenuous physical activities may not be advisable for patients with epidermolysis bullosa acquisita since this disease is exacerbated by trauma.

        

[drmithila]

Medication Summary
The treatment strategy for oral manifestations of autoimmune blistering diseases generally is the same as the treatment for the autoimmune blistering diseases themselves; therefore, please see Pemphigus Vulgaris, Bullous Pemphigoid, and Linear IgA Dermatosis for treatment options for those patients with these diseases who have oral involvement.

For cicatricial pemphigoid (mucous membrane pemphigoid) in which mucous membranes primarily are affected, the treatment strategy is discussed in detail in a separate article; therefore, the treatment for mucous membrane pemphigoid is not discussed herein. Adjunct treatments particularly relevant to oral lesions as a result of these autoimmune diseases are outlined below.

Anti-inflammatory agents
Class Summary
Used to treat oral lesions.

Clobetasol (Temovate)

Suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Class I superpotent topical steroid useful in treating oral lesions. Topical corticosteroids commonly are used intraorally for oral manifestations of autoimmune blistering skin diseases. Since these diseases are chronic inflammatory in nature, topical corticosteroids are very useful as an adjunct treatment. Patients with disease confined to the gingiva should see a dentist to have a custom-made soft tray to carry the medication.

Dapsone (Avlosulfon)

Mechanism of action is similar to that of sulfonamides, in which competitive antagonists of PABA prevent formation of folic acid, inhibiting bacterial growth. Anti-inflammatory mechanism of action remains unknown but probably relates to suppression of neutrophil function. Used alone or in conjunction with other anti-inflammatory medications or immunosuppressives for oral lesions.

Tetracycline (Sumycin)

Mechanism of action probably is by its anti-inflammatory properties, although it is an antibiotic by nature. Can be used alone or in conjunction with niacinamide.

Niacin (Vitamin B-3)

Source of niacin used in tissue respiration, lipid metabolism, and glycogenolysis.

        

[Drsumitra]

Further Inpatient Care
Inpatient care frequently is required for patients with the pemphigus group of diseases, particularly for those with pemphigus vulgaris and paraneoplastic pemphigus.

Further Outpatient Care
Regular follow-up care for patients with oral and skin manifestations of autoimmune blistering diseases by their dermatologists is recommended when the disease is active and during the tapering of medication when the disease is in remission.

Patients with oral autoimmune blistering disease alone should receive follow-up care from an oral medicine specialist for oral care treatment, otherwise poor oral hygiene will interfere with treatment outcome. Furthermore, complications from poor oral care could lead to periodontal disease and early teeth loss.

During the active disease stage, patient follow-up care every 4-6 weeks is recommended. Patients should be monitored for oral yeast infection. During the clinical remission stage, patient follow-up care every 6 months is recommended.

Transfer
Transferring patients with extremely severe disease with most of the skin denuded to a burn unit for close skin care may be indicated.

Deterrence/Prevention
Institute a combined supplement of calcium and vitamin D for patients treated with systemic corticosteroid for longer than 1 month to prevent osteoporosis. The guideline for dosage and frequency of this supplement is stated in the 1996 recommendations established by the American College of Rheumatology Task Force.

Institute a combined regimen of a non-alcohol–based mouthwash (Biotene mouthwash) and a weekly dose of systemic antifungal medication for patients at risk for oral candidiasis.

Complications
Monitoring treatment complications (eg, infection, osteoporosis, adrenal suppression) for patients receiving long-term immunosuppressive treatments is needed. If observed, treat complications properly.

Prognosis
The prognosis for patients with autoimmune blistering diseases generally is quite good. A small percentage of patients with pemphigus vulgaris do not respond well to treatment, which can lead to a fatal outcome. The prognosis for patients with paraneoplastic pemphigus is poor unless the associated primary neoplasm is found and eradicated.

Patient Education
Educate patients with autoimmune diseases about the nature of the disease and the possible adverse effects of long-term use of immunosuppressives. Also educate patients about the need for calcium and vitamin D supplements while using systemic corticosteroids. Finally, educate patients to monitor the signs and symptoms of infection in order to report possible complications to physicians in a timely manner.

        

[drmithila]

Bullous Impetigo is a cutaneous condition that characteristically occurs in the newborn, and is caused by a bacterial infection, presenting with bullae.
It can be caused by Exfoliative toxin A. The phyogenic superficial infection can be divided into two other subdivisions; Impetigo, and non-bullous impetigo. Bullous impetigo is caused by Staphylococcus aureus, which produces exfoliative toxins, whereas impetigo is caused by either Staphylococcus aureus, or Streptococcus.[3] Bullous Impetigo can cause deaths in fewer than 3% of infected children, but up to a 60% death rate in adults. 30% of all Impetigo cases are related to Bullous impetigoBullous impetigo can appear around the diaper region, axilla, or neck. The bacteria causes for a toxin to be produced with reduced cell-to-cell stickiness (adhesion), causing for the top layer of skin (epidermis), and lower layer of skin (dermis) top separate.[6] Vesicles rapidly enlarge and form the bullae which is a blister more than 5mm across. Bullae is also known as Staphylococcal scalded skin syndrome. Other associated symptoms are itching, swelling of nearby glands, fever and diarrhea. It should also be noted that pain is very rare.

Diagnosis
Observing the skins physical appearance, or swabbing a culture of the lesion for S. aureus. Nasal swabs from the patient’s immediate family members are necessary to identify them as being asymptomatic nasal carriers of S. aureus.
Long term effects: Once the scabs on the bullous have fallen off scarring is minimal. Possible long term effects are kidney disease
Possible misdiagnoses
HPV
insect bites
burns

 

        

[drmithila]

Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are two forms of a life-threatening skin condition, in which cell death causes the epidermis to separate from the dermis. The syndrome is thought to be[by whom?] a hypersensitivity complex that affects the skin and the mucous membranes. The majority of cases are idiopathic (without a known cause). The main known cause is certain medications, followed by infections and, rarely, cancers.
The medical literature agrees that Stevens–Johnson syndrome (SJS) can be considered a milder form of toxic epidermal necrolysis (TEN).[1] These conditions were first recognised in 1922.[2]
Both diseases can be mistaken for erythema multiforme.[citation needed] Erythema multiforme is sometimes caused by a reaction to a medication, but is more often a type III hypersensitivity reaction to an infection (caused most often by Herpes simplex) and is relatively benign. Although both SJS and TEN can also be caused by infections, they are most often adverse effects of medications.[citation needed] Their consequences are potentially more dangerous than those of erythema multiforme.[citation needed]
]Signs and symptoms

 

Mucosal desquamation in a person with Stevens–Johnson syndrome

Conjunctivitis (inflammation of eye and eyelid) in SJS
Stevens–Johnson syndrome (SJS) usually begins with fever, sore throat, and fatigue, which is misdiagnosed and usually treated with antibiotics. Ulcers and other lesions begin to appear in the mucous membranes, almost always in the mouth and lips but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient’s ability to eat or drink. Conjunctivitis of the eyes occurs in about 30% of children who develop SJS. A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet, but usually not the scalp.

Micrograph showing full thickness epidermal necrosis with a basket weave-like stratum corneum and separation of the dermis and epidermis. Skin biopsy. H&E stain.
SJS, like toxic epidermal necrolysis and erythema multiforme, are characterized by confluent epidermal necrosis with minimal associated inflammation. The acuity is apparent from the (normal) basket weave-like pattern of the stratum corneum.
Causes

Stevens–Johnson syndrome (SJS) is thought to arise from a disorder of the immune system.[3] The immune reaction can be triggered by infections, drugs, or medications.[citation needed] In some groups, drug reaction may be aggravated by genetic factors.
SJS can be caused by infections. It usually follows common infections such as herpes simplex virus, influenza, mumps, cat-scratch fever, histoplasmosis, Epstein-Barr virus, mycoplasma pneumoniae, or similar.
Medication/drugs
See also: List of SJS inducing substances
Although Stevens–Johnson Syndrome can be caused by viral infections, malignancies, or severe allergic reactions to medication, the leading cause appears to be the use of antibiotics and sulfa drugs.
SJS can be caused by adverse effects of drugs allopurinol, valproate, levofloxacin, diclofenac, etravirine, isotretinoin, fluconazole,[4] valdecoxib, sitagliptin, oseltamivir, penicillins, barbiturates, sulfonamides, phenytoin, azithromycin, oxcarbazepine, zonisamide, modafinil,[5] lamotrigine, nevirapine, pyrimethamine, ibuprofen, ethosuximide, carbamazepine, bupropion [1], and nystatin.
Medications that have traditionally been known to lead to SJS, erythema multiforme and toxic epidermal necrolysis include sulfonamides (antibiotics), penicillins (antibiotics), cefixime (antibiotic), barbituates (sedatives), lamotrigine, and phenytoin (e.g., Dilantin) (anticonvulsants). Combining lamotrigine with sodium valproate increases the risk of SJS.
Non-steroidal anti-inflammatory drugs are a rare cause of SJS in adults; the risk is higher for older patients, women and those initiating treatment.[2] Typically, the symptoms of drug-induced SJS arise within a week of starting the medication. People with systemic lupus erythematosus or HIV infections are more susceptible to drug-induced SJS.[3]
Genetics
In some East Asian populations studied (Han Chinese and Thai), carbamazepine- and phenytoin-induced SJS is strongly associated with HLA-B*1502 (HLA-B75), an HLA-B serotype of the broader serotype HLA-B15.[9][10][11] A study in Europe suggested that the gene marker is only relevant for East Asians.[12][13]
Based on the Asian findings, similar studies in Europe showed 61% of allopurinol-induced SJS/TEN patients carried the HLA-B58 (phenotype frequency of the B*5801 allele in Europeans is typically 3%). One study concluded: "Even when HLA-B alleles behave as strong risk factors, as for allopurinol, they are neither sufficient nor necessary to explain the disease."[14]
Treatment

SJS constitutes a dermatological emergency. All medications should be discontinued, particularly those known to cause SJS reactions. Patients with documented mycoplasma infections can be treated with oral macrolide or oral doxycycline.[3]
Initially, treatment is similar to that for patients with thermal burns, and continued care can only be supportive (e.g. intravenous fluids and nasogastric or parenteral feeding) and symptomatic (e.g., analgesic mouth rinse for mouth ulcer). Dermatologists and surgeons tend to disagree about whether the skin should be debrided.[3]
Beyond this kind of supportive care, there is no accepted treatment for SJS. Treatment with corticosteroids is controversial. Early retrospective studies suggested that corticosteroids increased hospital stays and complication rates. There are no randomized trials of corticosteroids for SJS, and it can be managed successfully without them.
Other agents have been used, including cyclophosphamide and cyclosporine, but none has exhibited much therapeutic success. Intravenous immunoglobulin (IVIG) treatment has shown some promise in reducing the length of the reaction and improving symptoms. Other common supportive measures include the use of topical pain anesthetics and antiseptics, maintaining a warm environment, and intravenous analgesics. An ophthalmologist should be consulted immediately, as SJS frequently causes the formation of scar tissue inside the eyelids, leading to corneal vascularization, impaired vision and a host of other ocular problems.
SJS proper (with less than 10% of body surface area involved) has a mortality rate of around 5%. The risk for death can be estimated using the SCORTEN scale, which takes a number of prognostic indicators into account.[15] Other outcomes include organ damage/failure, cornea scratching, and blindness

 

        

[drmithila]

Dental professionals should build a stronger connection between oral health and general health — not only for patients, but also at the community level, according to a special issue of this month’s Journal of Evidence-Based Dental Practice.

An editorial by Robert J. Collins, DMD, MPH, of the University of Pennsylvania, highlights the role of evidence-based innovations such as home dental care, community water fluoridation, and dental sealants in shifting public perceptions of dental care from replacement or repair of missing or damaged teeth to protection against oral diseases. Dr. Collins calls on dentists to recognize the value of collaboration in addressing the problems of the public and the dental profession.

Crossover topics in the issue include the following:

“Rubber cup” dental prophylaxis: There’s little evidence of a health benefit for this familiar “preventive” technique, but it continues to be widely used.
Prophylactic surgical extraction of third molars: Growing evidence questions the need for this procedure, although controversy continues.
Chlorhexidine mouthwash to reduce the risk of ventilator-associated pneumonia: an example of how better oral health can help prevent a serious medical condition, with important implications for dental care in nursing home residents.
The issue includes commentary by ADA President William Calnon, DDS. In contrast to its historical emphasis on surgical treatment of dental diseases after they have occurred — “drilling and filling” — Dr. Calnon believes the ADA and the dental profession at large need to develop a new framework for prevention of oral disease.

Editorials highlight the need for private dental practitioners to take on increased responsibility for carrying out essential public health functions and also the impact of financial incentives on the provision of evidence-based preventive services in clinical dentistry.

        

[Author]

Posts