Herpes Zoster

Varicella-zoster virus (VZV) is the agent causing varicella, otherwise known as chickenpox, the common childhood infection. Following resolution of chickenpox, VZV lies dormant in the spinal dorsal root ganglia until a decrease in cellular immunity triggers the reactivation of the virus, resulting in herpes zoster, otherwise known as shingles. 

Shingles is a syndrome characterized by a painful, vesicular rash that is usually restricted to a unilateral dermatomal distribution. At times, especially in the immunosuppressed patient, the infection may spread and produce severe systemic illness, with involvement of multiple visceral organs and multiple dermatomes (disseminated zoster). 

Shingles usually has a benign course, but complications may occur, ranging from mild to life threatening. In properly selected patients, early treatment with antivirals and corticosteroids has been shown to decrease the duration of symptoms and to possibly prevent or ameliorate some complications. 

The clinical manifestations of herpes zoster can be divided into the preeruptive phase (preherpetic neuralgia), acute eruptive phase, and chronic phase (postherpetic neuralgia).

VZV reactivation causes inflammation in the dorsal root ganglion, accompanied by hemorrhagic necrosis of nerve cells. The result is neuronal loss and fibrosis. The distribution of the rash corresponds to the sensory fields of the infected neurons within a specific ganglion. The anatomic location of the involved dermatome often determines the specific manifestations (eg, herpes zoster ophthalmicus [HZO], causing ocular complications, when the trigeminal ganglion is involved).

Pathophysiology-

Central nervous system involvement

While zoster is classically described in sensory (dorsal root) ganglia, it can spread to affect any portion of the nervous system.

Involvement of the anterior horn cells can produce muscular weakness, cranial nerve palsies, diaphragmatic paralysis, neurogenic bladder, and colon pseudo-obstruction.

Wider involvement of the spinal cord can produce Guillain-Barré syndrome, transverse myelitis, and myositis.

In severely ill or immunocompromised patients, general central nervous system (CNS) involvement can be observed in the form of meningoencephalitis or encephalitis. Such presentations are indistinguishable from other forms of meningoencephalitis, although other evidence of acute zoster usually is present.Cerebrospinal fluid (CSF) studies frequently reveal pleocytosis without elevated protein. These infections can be life threatening.

Herpes zoster ophthalmicus

This is potentially the most devastating form of acute zoster.

Herpes zoster ophthalmicus (HZO) results from the reactivation of varicella-zoster virus (VZV) in the trigeminal (fifth cranial) nerve. Any branch of the nerve may be affected, although the frontal branch within the first division of the trigeminal nerve is most commonly involved. This branch innervates nearly all of the ocular and periocular structures.

Ramsay Hunt syndrome

Also known as herpes zoster oticus, geniculate neuralgia, or herpes zoster auricularis, Ramsay-Hunt syndrome is caused by VZV reactivation involving the facial and auditory nerves. 

Vesicular eruptions may manifest on the pinna, tragus, or tympanic membrane or in the auditory canal, as well as anywhere in the facial nerve distribution.

The patient may experience hearing impairment, nystagmus, vertigo, or facial nerve palsy (mimicking Bell palsy).Patients may lose taste sensation in the anterior two thirds of the tongue.

Ramsay Hunt syndrome may go unnoticed and be difficult to diagnose, especially in elderly patients.

Etiology-

VZV is an enveloped, double-stranded deoxyribonucleic acid (DNA) virus belonging to the Herpesviridae family. In humans, primary infection with VZV occurs when the virus comes into contact with the mucosa of the respiratory tract or conjunctiva. From these sites, it is distributed throughout the body via mononuclear cells in the blood stream. In tissue, VZV spreads from cell to cell via direct contact to produce its effects.

After primary infection, the virus migrates along sensory nerve fibers to the satellite cells of dorsal root ganglia where it becomes dormant. This dormancy may be permanent, or the virus may become reactivated by conditions of decreased cellular immunity, resulting in herpes zoster.

Exactly why VZV reactivates from latency is not fully understood. However, cell-mediated, VZV-specific immunity has been shown to be a major factor in determining reactivation of VZV. Cell-mediated, VZV-specific immunity decreases with age and in patients with certain malignancies. These groups have much higher rates of herpes zoster. Patients with hypogammaglobulinemia (a defect of humoral, but not cellular, immunity) do not have a higher rate of zoster. This supports the concept of an important role for cell-mediated immunity in the pathogenesis of VZV infection.

No identifiable environmental, genetic, or social risk factors exist for the development of the reactivation of VZV.

Clinical Features-

Prodromal pain precedes the rash in approximately 70-80% of patients; it is typically confined to the same dermatomal distribution as the rash. In immunocompetent patients, herpes zoster is generally restricted to one dermatome, with possible limited involvement of adjacent dermatomes due to normal variations in innervation. Many patients describe the pain as "burning," "throbbing," or "stabbing." It may be severe, mild, constant, rare, or felt as another sensation such as pruritus. The involved area may be tender to palpation.

After 48-72 hours, or longer in some cases, the rash develops. Initially, and briefly, maculopapular lesions rapidly transition to vesicles in 1-2 days. New vesicles tend to form over 3-5 days, sometimes coalescing to form bullae. The lesions then rupture and release their contents, ulcerate, crust over, and dry, over 7-10 days. As with chickenpox, once crusting occurs, the lesions are no longer infectious.

Depending on the dermatome involved, additional physical examination findings may include the following:

• Corneal ulcers, conjunctivitis
• Regional lymphadenopathy
• Cranial nerve palsies
• Peripheral facial nerve palsy
• Delirium, confusion, coma (in patients with meningoencephalitis)
• Loss of taste in the anterior tongue (in Ramsay Hunt Syndrome)

Symptomatic involvement of multiple dermatomes or bilateral aspects of the same dermatome (ie, crossing the midline) may indicate disseminated disease or another etiology such as herpes simplex virus (HSV) infection.

Symptoms and lesions tend to resolve over 10-15 days. However, lesions may require up to 1 month to completely heal. Scarring and hyperpigmentation or hypopigmentation at lesion sites may persist for a long period or may be permanent. Pain duration is variable but is usually less than 1 month. Pain lasting longer than 1 month is referred to, by definition, as postherpetic neuralgia.

Less than 20% of patients have systemic symptoms, such as headache, fever, malaise, or fatigue, at any point during a case of herpes zoster.

Herpes zoster may develop without the typical rash, as aseptic meningitis or zoster sine herpete, which is a condition defined as pain and paresthesias along a dermatome without the development of visible cutaneous involvement

Treatment-

Episodes of herpes zoster are generally self-limited and resolve without intervention. However, effective treatments do exist and can reduce the extent and duration of symptoms, and possibly the risk of chronic sequelae (ie, postherpetic neuralgia) as well. Treatment is of most benefit in those patient populations at risk for prolonged or severe symptoms, specifically, immunocompromised people and persons older than 50 years. The benefit of treating younger and healthier populations is unclear.

Uncomplicated zoster does not require inpatient care. Patients at high risk for disseminated zoster may benefit from intravenous (IV) acyclovir. Patients with disseminated zoster usually require admission for IV acyclovir. Inpatient care is also recommended for any patient demonstrating disseminated disease or ophthalmic or meningoencephalopathic involvement.

The use of steroids in conjunction with an antiviral for uncomplicated herpes zoster is controversial.

The addition of oral corticosteroids has been evaluated in patients treated with acyclovir in 2 controlled studies. Steroids were found to accelerate the resolution of acute neuritis and provide a clear improvement in quality-of-life measures in comparison to those patients treated with antivirals alone. The use of oral steroids had no effect on the development or duration of postherpetic neuralgia. Oral steroids have not been studied with valacyclovir or famciclovir, so the benefit is unknown.

Nonoral forms of adjunctive steroid therapy in acute herpes zoster have also been studied. A study involving a single epidural injection of steroids and local anesthetics given in conjunction with a standard regimen of oral antivirals and analgesics was found to modestly improve zoster-associated pain for 1 month over treatment without steroids. As above, no effect in preventing postherpetic neuralgia was noted.

In light of the potential adverse effects of and contraindications to corticosteroid use, current expert opinion suggests limiting their involvement to cases of moderate to severe zoster pain, or in which significant neurological symptoms (such as facial paralysis) or CNS involvement is present (and use of corticosteroids is not otherwise contraindicated).

The optimal duration of steroid therapy is not known. If prescribed, it seems reasonable for steroids to be used concurrently with antiviral therapy. The duration of steroid use should not extend beyond the period of antiviral therapy. Steroids should not be given alone (without antiviral therapy), owing to concern about the promotion of viral replication.

Treatment of complicated herpes zoster-

Individuals with altered cell-mediated immunity, due to an immunosuppressive condition (eg, HIV, cancer) or treatment (eg, extended corticosteroid use), are at increased risk for herpes zoster. Further, herpes zoster presentations in the immunocompromised population can be complicated by disseminated disease and visceral organ involvement.

Antiviral therapy has been demonstrated to halt progression and dissemination of acute herpes zoster in immunocompromised patients, even when initiated more than 72 hours after rash onset.As such, current expert opinion recommends the use of antiviral therapy in all immunocompromised zoster patients who present prior to full crusting of all lesions.

Intravenous acyclovir remains the drug of choice for selected populations of immunocompromised patients, as follows:

• Patients with evidence of disseminated disease or visceral organ involvement
• Patients with ophthalmic involvement
• Patients with advanced HIV/AIDS with active opportunistic infections or prominent wasting
• Transplant recipients soon after transplantation or when being treated for rejection

Patients without such risk factors can be treated with oral antivirals. Data on adjunctive therapy with corticosteroids are lacking, and this therapy is not currently recommended. Antiviral therapy should be continued until resolution of all lesions.

Herpes simplex

Herpes simplex viruses are ubiquitous, host-adapted pathogens that cause a wide variety of disease states. Two types exist: herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2). Both are closely related but differ in epidemiology. HSV-1 is traditionally associated with orofacial disease, while HSV-2 is traditionally associated with genital disease; however, lesion location is not necessarily indicative of viral type.

Up to 80% of herpes simplex infections are asymptomatic. Symptomatic infections can be characterized by significant morbidity and recurrence. In immunocompromised hosts, infections can cause life-threatening complications.

Pathophysiology-

The prevalence of HSV infection worldwide has increased over the last several decades, making it a major public health concern. Prompt recognition of herpes simplex infection and early initiation of therapy are of utmost importance in the management of the disease.

HSV (both types 1 and 2) belongs to the family Herpesviridae and to the subfamily Alphaherpesvirinae. It is a double-stranded DNA virus characterized by the following unique biological properties

• Neurovirulence (the capacity to invade and replicate in the nervous system)
• Latency (the establishment and maintenance of latent infection in nerve cell ganglia proximal to the site of infection): In orofacial HSV infections, the trigeminal ganglia are most commonly involved, while, in genital HSV infection, the sacral nerve root ganglia (S2-S5) are involved.
• Reactivation: The reactivation and replication of latent HSV, always in the area supplied by the ganglia in which latency was established, can be induced by various stimuli (eg, fever, trauma, emotional stress, sunlight, menstruation), resulting in overt or covert recurrent infection and shedding of HSV. In immunocompetent persons who are at an equal risk of acquiring HSV-1 and HSV-2 both orally and genitally, HSV-1 reactivates more frequently in the oral rather than the genital region. Similarly, HSV-2 reactivates 8-10 times more commonly in the genital region than in the orolabial regions. Reactivation is more common and severe in immunocompromised individuals.

Dissemination of herpes simplex infection can occur in people with impaired T-cell immunity, such as in organ transplant recipients and in individuals withAIDS.

HSV is distributed worldwide. Humans are the only natural reservoirs, and no vectors are involved in transmission. Endemicity is easily maintained in most human communities owing to latent infection, periodic reactivation, and asymptomatic virus shedding.

HSV is transmitted by close personal contact, and infection occurs via inoculation of virus into susceptible mucosal surfaces (eg, oropharynx, cervix, conjunctiva) or through small cracks in the skin. The virus is readily inactivated at room temperature and by drying; hence, aerosol and fomitic spread are rare.

HSV-1 infections transmitted via saliva are common in children, although primary herpes gingivostomatitis can be observed at any age.

Clinical presentation-

The clinical course of herpes simplex infection depends on the age and immune status of the host, the anatomic site of involvement, and the antigenic virus type. Primary herpes simplex virus (HSV)–1 and HSV-2 infections are accompanied by systemic signs, longer duration of symptoms, and higher rate of complications. Recurrent episodes are milder and shorter. Both HSV-1 and HSV-2 can cause similar genital and orofacial primary infections after contact with infectious secretions containing either HSV-1 (usually oral secretions) or HSV-2 (usually genital secretions).

• Acute herpetic gingivostomatitis
  

  • This is a manifestation of primary HSV-1 infection that occurs in children aged 6 months to 5 years. Adults may also develop acute gingivostomatitis, but it is less severe and is associated more often with a posterior pharyngitis.
  • Infected saliva from an adult or another child is the mode of infection. The incubation period is 3-6 days.
  • Clinical features include the following:
    • Abrupt onset
    • High temperature (102-104°F)
    • Anorexia and listlessness
    • Gingivitis (This is the most striking feature, with markedly swollen, erythematous, friable gums.)
    • Vesicular lesions (These develop on the oral mucosa, tongue, and lips and later rupture and coalesce, leaving ulcerated plaques.)
    • Tender regional lymphadenopathy
    • Perioral skin involvement due to contamination with infected saliva
  • Course: Acute herpetic gingivostomatitis lasts 5-7 days, and the symptoms subside in 2 weeks. Viral shedding from the saliva may continue for 3 weeks or more.
• Acute herpetic pharyngotonsillitis
  

  • In adults, oropharyngeal HSV-1 infection causes pharyngitis and tonsillitis more often than gingivostomatitis.
  • Fever, malaise, headache, and sore throat are presenting features.
  • The vesicles rupture to form ulcerative lesions with grayish exudates on the tonsils and the posterior pharynx.
  • Associated oral and labial lesions occur in fewer than 10% of patients.
  • HSV-2 infection can cause similar symptoms and can be associated with orogenital contact or can occur concurrently with genital herpes.
• Herpes labialis/Cold sore
  

  • This is the most common manifestation of recurrent HSV-1 infection. A prodrome of pain, burning, and tingling often occurs at the site, followed by the development of erythematous papules that rapidly develop into tiny, thin-walled, intraepidermal vesicles that become pustular and ulcerate. In most patients, fewer than two recurrences manifest each year, but some individuals experience monthly recurrences.
  • Maximum viral shedding is in the first 24 hours of the acute illness but may last 5 days.

  
  

  
  

  Physical-

This section describes physical examination findings of the herpetic lesion as it relates to primary and recurrent lesions of cutaneous or mucosal HSV infection. This can be related to either oral or genital infection.

• Primary mucocutaneous HSV infections
  

  • Some primary infections are asymptomatic.
  • Primary (first-episode) infections manifest within several days of exposure to secretions containing viable virus.
  • Often painful, the lesions quickly progress to vesicles and can continue to erupt over 1-2 weeks.
  • The lesions are prominent and are often present internally on the mucosal surface of the oral or genital area, as well as on the surrounding skin.
  • Constitutional symptoms (fever, malaise, myalgias, and anorexia) are often prominent. Weight loss is not uncommon and is due either to illness or dysphagia (in primary gingivostomatitis).
  • Individual vesicles on mucosal surfaces break down rapidly, forming shallow painful ulcers (usually < 8-10 mm in diameter). They may be covered with a white exudate that can be confused with mucosal candidiasis. Those on cutaneous surfaces remain as vesicles longer, only to evolve into crusted ulcers that heal within 5-7 days.
• Recurrent mucocutaneous HSV infections
  

  • Following the establishment of latency in the corresponding sensory nerve ganglion cells, HSV can cause recurrent infection that can be subclinical (manifesting as viral excretion without lesions) or overt (manifesting as mucosal or cutaneous lesions with viral excretion).
  • Oral recurrences are often triggered by recognizable stimuli such as pyrexia (fever blisters and cold sores), stress, or sunburn. Genital recurrences are more likely to be linked to stress rather than to pyrexia. Females may relate a relationship to the menstrual cycle.
  • Localized burning or paraesthesias may precede recurrent lesions. Unlike primary infection, constitutional symptoms are minimal in most cases.
  • Recurrences last 3-7 days and can occur numerous times per year or once or twice in a lifetime. Overall, the number of yearly recurrences tends to decrease over time.
  • Although recurrent HSV infections may last much longer (>30 d) in immunocompromised hosts, such as individuals with AIDS, frequent recurrences are not necessarily a sign of an altered immune system.
  • Because recurrences can be clinically unrecognizable, transmission to susceptible individuals can occur in the absence of overt lesions. In genital HSV infections, barrier protection should be used regardless of existing lesions, even in the absence of a history of genital HSV infection.

  Causes-

  
  

  • HSV is transmitted via close personal contact.
  • HSV infection occurs via inoculation of virus into susceptible mucosal surfaces (eg, oropharynx, cervix, conjunctiva) or through small cracks in the skin.
  • The virus is inactivated readily at room temperature and by drying; hence, aerosol and fomitic spread are rare.
  • HSV-1 is transmitted chiefly by contact with infected saliva, whereas HSV-2 is transmitted sexually or from a mother's genital tract infection to her newborn. However, lesion location does not always indicate viral type.
    Treatment-
    Overall, medical treatment of herpes simplex virus (HSV) infection is centered around specific antiviral treatment. While the same medications are active against HSV-1 and HSV-2, the location of the lesions and the chronicity (primary or reactivation) of the infection dictate the dosage and frequency of medication. It is important to note that life-threatening HSV infections in immunocompromised patients and HSV encephalitis require high-dose intravenous acyclovir, often started empirically.

    When constitutional effects such as fever occur, symptomatic treatment can be used.

    Appropriate wound care is needed, and treatment for secondary bacterial skin infections may be required.

    Fluids can be given to avoid dehydration.

Oral lichen planus

Oral lichen planus (OLP) is a chronic inflammatory disease that causes bilateral white striations, papules, or plaques on the buccal mucosa, tongue, and gingivae. Erythema, erosions, and blisters may or may not be present. 

Pathophysiology-

Current data suggest that oral lichen planus is a T-cell–mediated autoimmune disease in which autocytotoxic CD8⁺ T cells trigger apoptosis of oral epithelial cells.

Oral lichen planus lesions contain increased levels of the cytokine tumor necrosis factor (TNF)–alpha.Basal keratinocytes and T cells in the subepithelial infiltrate express TNF in situ..

History-

The lichen planus antigen is unknown, although it may be a self-peptide (or altered self-peptide), in which case lichen planus would be a true autoimmune disease. The role of autoimmunity in the pathogenesis is supported by many autoimmune features of oral lichen planus, including its chronicity, onset in adults, predilection for females, association with other autoimmune diseases, occasional tissue-type associations, depressed immune suppressor activity in patients with oral lichen planus, and the presence of autocytotoxic T-cell clones in lichen planus lesions. The expression or unmasking of the lichen planus antigen may be induced by drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), viral infection, or other unidentified agents.


Clinical Features-

In many patients, the onset of oral lichen planus is insidious, and patients are unaware of their oral condition. In such instances, the referring medical or dental practitioner identifies the clinical changes in the oral mucosa.

Some patients report a roughness of the lining of the mouth, sensitivity of the oral mucosa to hot or spicy foods or oral hygiene products, painful oral mucosa, sore gums, red or white patches on the oral mucosa, red gums, or oral ulcerations.

Approximately two thirds of patients with oral lichen planus report oral discomfort, especially in association with atrophic and erosive lesions. Erythematous and erosive lesions are often sensitive or painful. Symptoms vary from mucosal sensitivity to continuous debilitating pain.

Oral mucosal lichenoid lesions may occur after the administration of systemic drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs), sulfonylureas, antimalarials, beta-blockers, and some angiotensin-converting enzyme (ACE) inhibitors. The period between the commencement of the drug therapy and the clinical appearance of oral lichen planus–like disease varies.

In rare cases, oral mucosal lichenoid lesions occur after a dental restoration is performed or after the patient starts using a denture; the lag period varies. Patients with an associated allergy to metals or components of the appliance should be evaluated by means of patch testing.

Up to 44% of patients with oral lichen planus develop coincident skin lesions. Conversely, more that 70% of patients with cutaneous lichen planus develop coincident oral lichen planus.

The genitals are involved in as many as 25% of women with oral lichen planus, compared with only 2-4% of men with oral lichen planus. The features are similar to those of the oral lesions. Patients do not often complain of pain or pruritus, although on questioning, they may admit to such symptoms.

In patients with oral lichen planus, scalp involvement (lichen planopilaris) is rare.

Nail involvement in patients with oral lichen planus is uncommon.

In a small group of patients, lichen planus may involve the esophagus.

Physical-

Pertinent physical findings in oral lichen planus are limited to the oral mucosa. Some patients present with coincident lesions on the skin, scalp, nails, genital mucosa, esophageal mucosa, larynx, and conjunctivae. Complete history taking and physical examination by a dermatologist may be required in patients with extra-oral symptoms or signs associated with oral lichen planus.

Patients with reticular lesions are often asymptomatic, whereas those with atrophic (erythematous) or erosive (ulcerative) disease commonly have significant local morbidity. The oral pain is variable and exacerbated by trauma and foods, particularly those that are hot, spicy, or acidic.

Oral mucosal lesions are variable and present as white striations (Wickham striae), white papules, white plaques, erythema (mucosal atrophy), erosions (shallow ulcers), or blisters. The lesions predominantly affect the buccal mucosa, tongue, and gingivae, although other oral sites are occasionally involved. The lesions are usually bilateral.

The lesions may appear as a mixture of clinical subtypes. For example, white streaks and gray streaks may form a linear or reticular pattern on an erythematous background. Alternatively, a central area of shallow ulceration (erosion) may have a yellowish surface (fibrinous exudate) surrounded by an area of erythema.

In most patients, telltale white striations or papules are evident on the buccal mucosa or on the lateral margin of the tongue, either alone or in combination with other lesions.

Gingival lesions commonly appear with a fiery red erythema that affects the entire width of the attached gingiva, a condition previously called desquamative gingivitis.

In patients predisposed to pigmentation, oral lichen planus lesions may be associated with patchy brown melanin deposits in the oral mucosa (inflammatory melanosis).

Oral lichen planus lesions usually persist for many years with periods of exacerbation and quiescence. During periods of exacerbation, the area of erythema or erosion increases, with increased pain and sensitivity. During periods of quiescence, the area of erythema or erosion decreases, with decreased pain and sensitivity. Patients are often unaware of quiescent oral lichen planus, which may manifest as faint white striations, papules, or plaques. Exacerbations of oral lichen planus have been linked to periods of psychological stress and anxiety.

Lichenoid drug reactions have the same clinical features as those of idiopathic oral lichen planus. Lichenoid disease may be unilateral and associated with circulating epithelial antinuclear antibodies, but few data support this possibility. Rarely, lichenoid reactions of the oral mucosa occur on the oral mucosa in contact with (or close to) an amalgam or composite resin dental restoration, or a denture component. Mechanical trauma (the Koebner phenomenon) may exacerbate lichenoid lesions, especially when it affects the midline of the buccal mucosa or the lateral margin of the tongue.

Up to 44% of patients with oral lichen planus develop coincident skin lesions. These typically appear as pruritic, flat-topped, violaceous papules and plaques that predominantly affect the flexor aspects of the wrists or ankles, the extensor aspects of the lower legs, the skin of the lower central part of the back, and the natal cleft.

Causes-

Current data suggest that oral lichen planus is a T-cell–mediated autoimmune disease in which autocytotoxic CD8⁺ T cells trigger the apoptosis of oral epithelial cells. However, the precise cause of oral lichen planus is unknown.

In many patients, a cause for the oral lichenoid lesions cannot be identified; in these patients, the disease is called idiopathic oral lichen planus.

Oral lichenoid drug reactions may be triggered by systemic drugs including NSAIDs, beta-blockers, sulfonylureas, some ACE inhibitors, and some antimalarials. In patients with oral lichenoid lesions, be alert for any systemic drug as a cause.

Oral lichenoid contact-sensitivity reactions may be triggered by contact allergens including dental amalgam composite resin, and toothpaste flavorings, especially cinnamates. Skin patch testing may help in identifying contact allergens (see Other Tests). If an allergy is detected, lesions may heal when the offending material is removed.

Oral lichenoid lesions may be triggered by mechanical trauma (Koebner phenomenon) due to calculus deposits, sharp teeth, rough surfaces of dental restorations or prostheses, cheek or tongue biting, and oral surgical procedures. Scale any teeth associated with oral lichen planus lesions to remove calculus deposits and reduce sharp edges. Dental restorations and prostheses that are associated with oral lichen planus lesions should be mirror-polished.

Some studies have revealed viral infections in oral lichen planus, including those due to human papillomavirus (HPV-6, 11, 16, or 18) and human herpesvirus 6. A causal role for viral infection in oral lichen planus has not been identified.

Some studies show an increased incidence of C albicans infection in oral lichen planus. A causal role for C albicans infection in oral lichen planus has not been identified.

Some study findings suggest an association between oral lichen planus and chronic hepatic diseases such as hepatitis C virus (HCV) infection, autoimmune chronic active hepatitis, and primary biliary cirrhosis. 

Oral lichenoid lesions may arise in people who habitually chew betel quid. A causal role for betel quid in oral lichen planus has not been identified.

Oral lichenoid lesions are part of the spectrum of chronic graft-versus-host disease that occurs after allogeneic hemopoietic stem cell transplantation.

No consistent association with human leukocyte antigen (HLA) is reported in oral lichen planus. This finding suggests that the patient's genetic background does not play a critical role in oral lichen planus pathogenesis.

Little evidence supports a connection between diabetes mellitus and oral lichen planus. The oral lichenoid lesion in Grinspan syndrome (triad of oral lichen planus, diabetes mellitus, and hypertension) is probably an adverse effect of the drug therapy for diabetes mellitus and hypertension.

Hitopathology-

Histopathologic examination of lesional tissue is the most relevant investigation in cases of oral lichen planus.Consistent findings include a bandlike subepithelial mononuclear infiltrate consisting of T cells and histiocytes, increased numbers of intraepithelial T cells, and degenerating basal keratinocytes that form colloid (Civatte, hyaline, cytoid) bodies, which appear as homogenous eosinophilic globules. Variable findings include parakeratosis, acanthosis, and sawtooth rete pegs.

Degeneration of the basal keratinocytes and disruption of the anchoring elements of the epithelial basement membrane and basal keratinocytes (eg, hemidesmosomes, filaments, fibrils) weakens the epithelial-connective tissue interface. As a result, histologic clefts (ie, Max-Joseph spaces) may form, and blisters on the oral mucosa (bullous lichen planus) may be seen at clinical examination. B cells and plasma cells are uncommon findings.

Treatment-

Medical treatment of oral lichen planus (OLP) is essential for the management of painful, erythematous, erosive, or bullous lesions. The principal aims of current oral lichen planus therapy are the resolution of painful symptoms, the resolution of oral mucosal lesions, the reduction of the risk of oral cancer, and the maintenance of good oral hygiene. In patients with recurrent painful disease, another goal is the prolongation of their symptom-free intervals.

The main concerns with the current therapies are the local and systemic adverse effects and lesion recurrence after treatment is withdrawn. No treatment of oral lichen planus is curative.

Eliminate local exacerbating factors. Treat any sharp teeth or broken restorations or prostheses that are likely to cause physical trauma to areas of erythema or erosion by using conventional dental means. Scale the teeth to remove calculous deposits and reduce sharp edges. If the patient has an isolated plaquelike or erosive oral lichen planus lesion on the buccal or labial mucosa adjacent to a dental restoration, and if an allergy is detected by means of skin patch testing, the lesion may heal if the offending material is removed or replaced. (However, most lichenoid lesions adjacent to dental restorations are asymptomatic.)

If systemic drug therapy (eg, treatment with NSAIDs, antimalarials, or beta-blockers) is suspected as the cause of oral lichenoid lesions, changing to another drug may be worthwhile. This change must be undertaken only by the patient's attending physician. However, the switch rarely resolves the erosions, and almost never resolves the white patches of oral lichen planus.

Inform all patients with oral lichen planus about their slightly increased risk of oral SCC (the most common of all oral malignancies). As with all patients, advise those with oral lichen planus that this risk may be reduced by eliminating tobacco and alcohol consumption and by consuming a diet rich in fresh fruits and vegetables, among other measures. Erosive and atrophic lesions can be converted into reticular lesions by using topical steroids. Therefore, the elimination of mucosal erythema and ulceration, with a residual asymptomatic reticular or papular lesions, may be considered an end point of current oral lichen planus therapy. With respect to plaque lesions, the effect of treatment on the risk of oral cancer is unclear.

Topical corticosteroids are the mainstay of medical treatment of oral lichen planus, although rarely, corticosteroids may be administered intralesionally or systemically. Some topical corticosteroid therapies may predispose the patient to oral pseudomembranous candidosis. However, this condition is rarely if ever symptomatic, and it generally does not complicate healing of the erosions related to oral lichen planus. Topical antimycotics (eg, nystatin, amphotericin) may be prescribed when an infection is present.

Erosive oral lichen planus that is recalcitrant to topical corticosteroids may respond to topical tacrolimus. Other potential therapies for recalcitrant oral lichen planus include hydroxychloroquine, azathioprine, mycophenolate, dapsone, systemic corticosteroids, and topical and systemic retinoids.

Oral Candidiasis-II

What is oral thrush?

Thrush is an infection caused by a yeast germ called Candida spp. The mouth is a common site whereCandida spp. causes infection. Candidal infection in the mouth is called oral thrush. 

Who gets oral thrush?

Small numbers of Candida spp. commonly live on healthy skin and in a healthy mouth. They are usually harmless. Healthy people do not normally get oral thrush. However, certain situations or conditions may cause an overgrowth of Candida spp. which can lead to a bout of oral thrush. These include:

• Being a baby. Oral thrush is quite common in young babies.
• Wearing dentures, especially if they are not taken out at night, not kept clean, or do not fit well and rub on the gums.
• A course of antibiotics. Antibiotics will kill harmless bacteria which live in the mouth. They do not kill Candida spp. which may multiply more easily if there are fewer bacteria around.
• Excessive use of antibacterial mouthwash (for similar reasons to above).
• Taking steroid tablets or inhalers.
• Having a dry mouth due to a lack of saliva. This may occur as a side-effect from certain drugs (such as antidepressants, antipsychotics, chemotherapy), following radiotherapy to the head or neck, or as a symptom of Sjögren's syndrome.
• Having diabetes.
• Having severe anaemia.
• Lacking iron, folate or vitamin B12.
• Having a poor immune system. For example, if you are taking medicines that suppress your immune system, if you have certain cancers, or if you have HIV/AIDS.
• Being frail or in generally poor health.
• Smoking. Smokers are more likely to develop oral thrush.

Oral thrush is not contagious. You cannot pass on oral thrush to other people.

What are the symptoms of oral thrush?

• The classical symptom is white spots that develop in your mouth. The spots may join together to form larger spots called plaques. They may become yellow or grey. If you wipe off a spot, the underlying tissue may be red but it is not usually sore or painful.
• Often there are no white spots. Areas in your mouth may just become red and sore. This more typically occurs if you get thrush after taking antibiotics or steroids.
• Denture wearers may develop an area of persistent redness under a denture.
• You may develop sore, cracked, red areas just outside your mouth. This mainly affects the angle where the upper and lower lips meet (angular stomatitis).
• Some mild oral thrush infections are painless. However, sometimes oral thrush is quite sore and can make eating and drinking uncomfortable. Some babies with oral thrush may drool saliva, or not be able to feed properly because of soreness.
• Taste can be affected in some people with oral thrush.

How is oral thrush diagnosed?

Doctor will usually diagnose oral thrush by typical symptoms and the typical appearance in mouth. No investigations are usually needed to diagnose oral thrush.

However,doctor may sometimes suggest a blood test to look for certain conditions that may make you more likely to develop oral thrush. For example, a blood test to see if you are lacking iron, B12 or folate.

If oral thrush does not respond to treatment (see below), your doctor may suggest that they take a swab from inside your mouth. The swab is then sent to the laboratory to be examined under a microscope. They can also try to grow the Candida spp. in the laboratory.

Occasionally, a biopsy is needed to confirm a diagnosis of oral thrush. A small sample is taken from the white patches inside your mouth and this can be examined under a microscope.

What is the treatment for oral thrush?

Locally applied treatment

For mild oral thrush, the usual treatment that is tried first is miconazole mouth gel for seven days. Sometimes a two-week course is needed. Nystatin drops are another option if miconazole gel cannot be used (for example, if you are known to be allergic to it). 

Follow the instructions in the packet. Basically:

• The gel or drops should be used after you have eaten or drunk.
• Smear a small amount of gel on to the affected areas, with a clean finger, four times a day.
• With the drops, you use a dropper to place the liquid inside your mouth on to the affected areas four times a day.
• Ideally, you should not eat or drink for about 30 minutes after using either the gel or the drops. This helps to prevent the drug from being washed out of your mouth too soon.

Anti-thrush tablets

Tablets that contain a drug called fluconazole can also help to clear fungal and thrush infections from the body. Tablets tend to be used in more severe or serious cases. For example, for people with a poor immune system who develop extensive oral thrush. Tablets are usually prescribed for seven days and this will usually clear oral thrush.

Adjustment of other medication

If you are taking other medication that may have caused oral thrush, such as steroids or antibiotics, your doctor may need to change this medication or reduce the dose to help clear up your thrush.

Other drugs such as itraconazole, ketoconazole or amphotericin can also be used if above drug regime doesn't succeed.

Can oral thrush be prevented?

It may be possible to alter one or more of the situations mentioned above to help prevent further bouts of oral thrush. For example:

• If you have diabetes - good control of your blood sugar level reduces the risk of thrush and other infections.
• If you use steroid inhalers - having a good inhaler technique and using a spacer device may reduce the risk of thrush. Also, rinse your mouth after using the inhaler, to help remove any drug particles left in your mouth. Ask your doctor about reducing your dose of steroid in your inhaler to the lowest level needed to control your asthma.
• If you wear dentures:
  • Leave your dentures out overnight, or for at least six hours daily. Constant wearing of dentures, and not taking them out at night, is thought to be one of the most common causes of oral thrush.
  • Clean and disinfect dentures daily. To clean, use soapy water and scrub the dentures with a soft nailbrush on the fitting surface - that is, the non-polished side. Then soak them in a disinfecting solution. The type of solution and the time they should be soaked for will be advised by your dentist. Rinse the dentures after disinfecting them, and then allow the dentures to air dry before wearing them again. Drying like this helps to kill any Candida spp. that might be stuck to the dentures.
  • Clean the inside of your mouth (where the dentures sit) with a soft brush.
  • See a dentist if the dentures do not fit well.
• If you take medication which causes a dry mouth - take frequent sips of water. (See separate leaflet called 'Dry Mouth' for more details.)
• If you are found to have anaemia or low levels of vitamin B12, folate or iron, treating this may help to prevent oral thrush in the future.
• If you are a smoker, quitting smoking may help to prevent further bouts of oral thrush.
• Certain groups of people may be given anti-thrush tablets to help to prevent oral thrush. For example, people who are on medication to suppress their immune system or who are receiving chemotherapy for cancer.

ORAL CANDIDIASIS (MONILIASIS, THRUSH)-I

Candida albicans is the most frequent cause of fungal human disease in general and very much the most common cause of oral fungal involvement. The organism is a normal inhabitant of the oral cavity in 30 to 40% of the population. When the bacterial flora of the oral cavity is disturbed by antibiotic therapy, or in individuals who have diabetes mellitus, xerostomia (dry-mouth), weakened immunity (for example, AIDS), or severe debilitation, this otherwise harmless microorganism multiplies to cause overt lesions.

The causes and the course the disease:

Oral Candidiasis takes the form of a superficial, curdy, gray to white membrane that can be readily scraped off to reveal an underlying erythematous inflammatory base. In the milder expressions, there is minimal ulceration of the mucosal surface and only a superficial subepithelial inflammatory infiltrate. More severe oral infections may produce mucosal ulceration and a correspondingly greater inflammatory reaction.

In the debilitated, compromised host, the oral candidal infection may be spread into the esophagus by the introduction of a nasogastric tube. Even more threatening, in the vulnerable individual, is more widespread mucous-membrane infection with invasion of the fungi into the deeper tissues of the oral cavity, increasing the potential for bloodstream diffusion. Uncommonly, and in the vulnerable individual, oral candidiasis is followed by widespread mucous membrane infection that has greater potential for invasion and distribution.

The clinical features:

The patient with candidiasis may complain of a burning sensation, tenderness, or sometimes pain around the affected mucosa. Spicy foods will cause occasional discomfort because of the increased sensitivity of the affected mucosa. These infections were more common in women and in patients over 40 years old. Fifty percent of the patients came to them with a chief complaint of oral burning. The patient may report having been on a prolonged course of broad-spectrum antibiotics for a sore throat or other infection.

About oral candidiasis, four major types are recognized: (1) pseudomembranous; (2) hyperplastic; (3) erythematous (atrophic); and (4) angular cheilitis.

The pseudomembranous oral infection may show as fine whitish deposits on an ervthematous patch of mucosa or as more highly developed small, soft, white, slightly raised plaques that closely resemble to milk curds. The disease may range in severity from a single region to a diffuse whitish involvement of several or all the mucosal surfaces. The mucosa next to, or between, these whitish plaques appears red and moderately swollen. The plaques or pseudomembranes may be stripped off the mucosa, leaving a raw bleeding surface. When separate restricted sites are involved, the cheek mucosa and vestibule are the most frequent regions affected—followed by the dorsum of the tongue, palate, gum, floor of the mouth, and lips.

The hyperplastic type is characterized by white plaques which cannot be removed by scraping. The most common location is the cheek mucosa. In patients infected with HIV, the hyperplastic candidiasis most often is found in the lip commissures.

The erythematous (atrophic) type is characterized by a red appearance. The color intensity may vary from fiery red to a hardly distinct pink spot. Common locations are the palate and dorsum of the tongue, as in the so-called multifocal candidiasis in patients who are not infected with HIV but who are heavy smokers. However, erythematous candidiasis may also appear as spotty areas of the cheek mucosa. This is a characteristic feature of the HIV infection, but is often overlooked.

Angular cheilitis is characterized by cracks radiating from the angles of the mouth, often associated with small white plaques.  In the elderly, this is not an unusual lesion and may be because of anemia, loss of chewing vertical dimension, or vitamin deficiency. But it should be remembered that when it is noted in a young man, it could be the first sign of an HIV infection. Today it is recognized the most important etiologic cause is Candida albicans. However, Staphylococcus aureus may also be present in some patients.

The differential diagnosis:

The diagnosis of candidiasis relies on the clinical features and the presence of Candida hyphae on smears examined by potassium hydroxide, periodic acid-Schiff or Gram stain.

As a rule all the keratotic lesions may be readily ruled out from consideration, since they cannot be easily removed by scraping. Necrotic white lesions that must be considered in the differential diagnosis are chemical burns, gangrenous stomatitis, superficial bacterial infections, traumatic ulcers, necrotic ulcers of systemic disease, and the mucous patch.

The mucous patch of syphilis is usually a discrete, small, white necrotic lesion on the tongue, palate, or lips, whereas candidiasis is usually much more diffuse. The accompanying skin lesions of secondary syphilis and the positive serologic findings readily distinguish the mucous patch from candidiasis.

Necrotic ulcers and gangrenous stomatitis of debilitating systemic disease may be difficult to differentiate from candidiasis because the latter entity is usually also found in patients with undermining secondary disease. As a general rule, if the ulcer is deep then candidiasis would not be the primary cause. Traumatic ulcers with necrotic surfaces can often be related to a history of specific trauma. Chemical burns sometimes closely mimic candidiasis. The distinction is usually made by an accurate history, disclosing that a medicament has been applied to the mucosa.

Superficial bacterial infections may occur in patients with debilitating disease and indeed may mimic pseudomembranous candidiasis. Culture of these lesions yielded generous bacteria such as staphylococci, Neisseria, coliform bacteria, and lactobacilli.

The recommended treatment:

The management of patients with oral candidiasis is twofold: (1) to identify, correct, or eliminate predisposing or precipitating causes and (2) to provide antifungal therapy.

The underlying systemic conditions (such as diabetes, malnutrition, and anemia) and the discontinuation of broad-spectrum antibiotics are recommended for the first approaches. Local resistance can be improved by good oral hygiene and by leaving dentures out as much as possible.

The six drugs that are chiefly used for antifungal therapy are gentian violet, nvstatin, amphotericin B, miconazole, clotrimazole, and ketoconazole. Nystatin and amphotericin have been the standard drugs used for oral candidal infections for the last 35 years. Each of these drugs is absorbed poorly from the gastrointestinal tract but is excellent for topical use on mucous membrane and skin lesions.  Most dentists and physicians stress the importance of continuing antifungal therapy at least 2 weeks following disappearance of signs and symptoms of oral lesions.

CEMENTAL TEAR

Definition- A small portion of cementum separated, either partially or completely, from the underlying dentin of the root as a result of occlusive force or due to ageing wear out.
Etiology-Heavy occlusive forces or age
Clinical Feature-

• Generally seen w.r.t anterior teeth
• Deep Periodontal pockets (up to 11mm)
• Angular bone loss
• Vital Pulp
• Periodontal pockets exist only in relation to a single tooth and otherwise the whole of the gingiva can be healthy with no deep pockets

Its must to differentiate cemental tears from peripaical/periodontal pathologies.Dentist should avoid unnecessary RCT.Xrays taken at different angulations and pulp vitality help to differentiate.