Docosanol, a saturated fatty alcohol, is a safe and effective topical application that has been approved by the United States Food and Drug Administration for herpes labialis in adults with properly functioning immune systems. It is comparable in effectiveness to prescription topical antiviral agents. Due to its mechanism of action, there is little risk of drug resistance. The duration of symptoms can be shortened a bit if an antiviral, anesthetic, zinc oxide or zinc sulfate cream is applied soon after it starts.

Effective antiviral medications include acyclovir and penciclovir, which can speed healing by as much as 10%. Famciclovir or valacyclovir, taken in pill form, can be effective using a single day, high-dose application and is more cost effective and convenient than the traditional treatment of lower doses for 5–7 days.

Treatment includes fluid intake, good oral hygiene and gentle debridement of the mouth, as well as oral acyclovir. In healthy individuals the lesions heal spontaneously in 7–14 days without scarring.

No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and paracetamol (acetaminophen) can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine, or tetracaine can also relieve itching and pain.

Several antiviral drugs are effective for treating herpes, including acyclovir, valaciclovir (valacyclovir), famciclovir, and penciclovir. Acyclovir was the first discovered and is now available in generic. Valacyclovir is also available as a generic and is slightly more effective than aciclovir for reducing lesion healing time.

Evidence supports the use of acyclovir and valacyclovir in the treatment of herpes labialis as well as herpes infections in people with cancer. The evidence to support the use of acyclovir in primary herpetic gingivostomatitis is weaker.

The first line therapy for aphthous stomatitis is topical agents rather than systemic medication, with topical corticosteroids being the mainstay treatment. Systemic treatment is usually reserved for severe disease due to the risk of adverse side effects associated with many of these agents. A systematic review found that no single systemic intervention was found to be effective. Good oral hygiene is important to prevent secondary infection of the ulcers.

Occasionally, in females where ulceration is correlated to the menstrual cycle or to birth control pills, progestogen or a change in birth control may be beneficial. Use of nicotine replacement therapy for people who have developed oral ulceration after stopping smoking has also been reported. Starting smoking again does not usually lessen the condition. Trauma can be reduced by avoiding rough or sharp foodstuffs and by brushing teeth with care. If sodium lauryl sulfate is suspected to be the cause, avoidance of products containing this chemical may be useful and prevent recurrence in some individuals. Similarly patch testing may indicate that food allergy is responsible, and the diet modified accordingly. If investigations reveal deficiency states, correction of the deficiency may result in resolution of the ulceration. For example, there is some evidence that vitamin B12 supplementation may prevent recurrence in some individuals.

The vast majority of people with aphthous stomatitis have minor symptoms and do not require any specific therapy. The pain is often tolerable with simple dietary modification during an episode of ulceration such as avoiding spicy and acidic foods and beverages. Many different topical and systemic medications have been proposed (see table), sometimes showing little or no evidence of usefulness when formally investigated. Some of the results of interventions for RAS may in truth represent a placebo effect. No therapy is curative, with treatment aiming to relieve pain, promote healing and reduce the frequency of episodes of ulceration.

Although it is a self-limited illness, oral or intravenous antiviral treatments, particularly acyclovir, have been used in the management of immunocompromised or severely infected patients. Topical acyclovir has not been shown to be effective in management of herpetic whitlow. Famciclovir has been demonstrated to effectively treat and prevent recurrent episodes. Lancing or surgically debriding the lesion may make it worse by causing a superinfection or encephalitis.

The likelihood of the infection being spread can be reduced through behaviors such as avoiding touching an active outbreak site, washing hands frequently while the outbreak is occurring, not sharing items that come in contact with the mouth, and not coming into close contact with others (by avoiding kissing, oral sex, or contact sports).

Because the onset of an infection is difficult to predict, lasts a short period of time and heals rapidly, it is difficult to conduct research on cold sores. Though famciclovir improves lesion healing time, it is not effective in preventing lesions; valaciclovir and a mixture of acyclovir and hydrocortisone are similarly useful in treating outbreaks but may also help prevent them.

Acyclovir and valacyclovir by mouth are effective in preventing recurrent herpes labialis if taken prior to the onset of any symptoms or exposure to any triggers. Evidence does not support L-lysine.

Treatment is cause-related, but also symptomatic if the underlying cause is unknown or not correctable. It is also important to note that most ulcers will heal completely without any intervention. Treatment can range from simply smoothing or removing a local cause of trauma, to addressing underlying factors such as dry mouth or substituting a problem medication. Maintaining good oral hygiene and use of an antiseptic mouthwash or spray (e.g. chlorhexidine) can prevent secondary infection and therefore hasten healing. A topical analgesic (e.g. benzydamine mouthwash) may reduce pain. Topical (gels, creams or inhalers) or systemic steroids may be used to reduce inflammation. An antifungal drug may be used to prevent oral candidiasis developing in those who use prolonged steroids. People with mouth ulcers may prefer to avoid hot or spicy foods, which can increase the pain. Self-inflicted ulceration can be difficult to manage, and psychiatric input may be required in some people.

, genital herpes cannot be cured. There are, however, some medications that can shorten outbreaks including acyclovir, valacyclovir, and famciclovir.

Acyclovir is an antiviral medication and reduces the pain and the number of lesions in the initial case of genital herpes. Furthermore, it decreases the frequency and severity of recurrent infections. It comes in capsules, tablets, suspension, injection, powder for injection, and ointment. The ointment is used topically and it decreases pain, reduces healing time, and limits the spread of the infection.

Valacyclovir once in the body, it is converted to acyclovir. It helps relieve the pain and discomfort and the sores heal faster. It only comes in caplets and its advantage is that it has a longer duration of action than acyclovir. An example usage is by mouth twice per day for 10 days for primary lesion, and twice per day for 3 days for a recurrent episode.

Famciclovir is another antiviral drug that belongs to the same class. Famciclovir is a prodrug that is converted to penciclovir in the body. The latter is the one active against the viruses. It has a longer duration of action than acyclovir and it only comes in tablets.

When "H. pylori" infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. clarithromycin, amoxicillin, tetracycline, metronidazole) and a proton-pump inhibitor (PPI), sometimes together with a bismuth compound. In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin + metronidazole) may be used together with a PPI and sometimes with bismuth compound. An effective first-line therapy for uncomplicated cases would be amoxicillin + metronidazole + pantoprazole (a PPI).

H2 antagonists or proton-pump inhibitors decrease the amount of acid in the stomach, helping with healing of ulcers.

Epithelial keratitis is treated with topical antivirals, which are very effective with low incidence of resistance. Treatment of the disease with topical antivirals generally should be continued for 10–14 days. Aciclovir ophthalmic ointment and Trifluridine eye drops have similar effectiveness but are more effective than Idoxuridine and Vidarabine eye drops. Oral acyclovir is as effective as topical antivirals for treating epithelial keratitis, and it has the advantage of no eye surface toxicity. For this reason, oral therapy is preferred by some ophthalmologists.

Ganciclovir and brivudine treatments were found to be equally as effective as acyclovir in a systematic review.

Valacyclovir, a pro-drug of acyclovir likely to be just as effective for ocular disease, can cause thrombotic thrombocytopenic purpura/Hemolytic-uremic syndrome in severely immunocompromised patients such as those with AIDS; thus, it must be used with caution if the immune status is unknown.

Topical corticosteroids are contraindicated in the presence of active herpetic epithelial keratitis; patients with this disease who are using systemic corticosteroids for other indications should be treated aggressively with systemic antiviral therapy.

The effect of interferon with an antiviral agent or an antiviral agent with debridement needs further assessment.

Herpetic stromal keratitis is treated initially with prednisolone drops every 2 hours

accompanied by a prophylactic antiviral drug: either topical antiviral or an oral agent such as acyclovir or valacyclovir. The prednisolone drops are tapered every 1–2 weeks depending on the degree of clinical improvement. Topical antiviral medications are not absorbed by the cornea through an intact epithelium, but orally administered acyclovir penetrates an intact cornea and anterior chamber. In this context, oral acyclovir might benefit the deep corneal inflammation of disciform keratitis.

The goal of treatment is to reduce inflammation. Treatment usually does not require hospitalization unless tongue swelling is severe. Good oral hygiene is necessary, including thorough tooth brushing at least twice a day, and flossing at least daily. Corticosteroids such as prednisone may be given to reduce the inflammation of glossitis. For mild cases, topical applications (such as a prednisone mouth rinse that is not swallowed) may be recommended to avoid the side effects of swallowed or injected corticosteroids. Antibiotics, antifungal medications, or other antimicrobials may be prescribed if the cause of glossitis is an infection. Anemia and nutritional deficiencies (such as a deficiency in niacin, riboflavin, iron, or Vitamin E) must be treated, often by dietary changes or other supplements. Avoid irritants (such as hot or spicy foods, alcohol, and tobacco) to minimize the discomfort.

In some cases, tongue swelling may threaten the airway, a medical emergency that needs immediate attention.

The need for medications to prevent stress ulcer among those in the intensive care unit is unclear. As of 2014, the quality of the evidence is poor. It is unclear which agent is best or if prevention is needed at all. Benefit may only occur in those who are not being fed.

Possible agents include antacids, H2-receptor blockers, sucralfate, and proton pump inhibitors (PPIs). Tentative evidence supports that PPIs may be better than H2 blockers.

Concerns with the use of stress ulcer prophylaxis agents include increased rates of pneumonia and "Clostridium difficile" colitis.

Treatment is usually supportive only, as the disease is self-limiting and usually runs its course in less than a week.

The principles of management are the same as for the chronic ulcer. The steps of management are similar as in erosive gastritis.

Endoscopic means of treating stress ulceration may be ineffective and operation required. It is believed that shunting of blood away from the mucosa makes the mucous membrane ischaemic and more susceptible to injury.

Treatment of stress ulceration usually begins with prevention. Careful attention to respiratory status, acid-base balance, and treatment of other illnesses helps prevent the conditions under which stress ulcers occur. Patients who develop stress ulcers typically do not secrete large quantities of gastric acid; however, acid does appear to be involved in the pathogenesis of the lesions. Thus it is reasonable either to neutralize acid or to inhibit its secretion in patients at high risk.

In case of severe hemorrhagic or erosive gastritis and stress ulcers, a combination of antacids and H2-blockers may stop active bleeding and prevent re bleeding. In selected patients, either endoscopic therapy or selective infusion of vasopressin into the left gastric artery may help control the hemorrhage.

Antacids are a common treatment for mild to medium gastritis. When antacids do not provide enough relief, medications such as H blockers and proton-pump inhibitors that help reduce the amount of acid are often prescribed.

Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. They include the medications sucralfate and misoprostol. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate.

Several regimens are used to treat "H. pylori" infection. Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is added to the regimen.

Testing peoples blood, including those who are pregnant, who do not have symptoms for HSV is not recommended. This is due to concerns of greater harm than benefit such as relationship problems in the setting of a high rate of tests that may be falsely positive.

The natural history of postherpetic neuralgia involves slow resolution of the pain syndrome. Most people who develop postherpetic neuralgia respond to agents such as tricyclic antidepressants. A subgroup of affected individuals may develop severe, long-lasting pain that does not respond to medical therapy.

An April 2013 Cochrane Collaboration meta-analysis of 6 randomized controlled trials (RCTs) investigating oral antiviral medications given within 72 hours after the onset of herpes zoster rash in immunocompetent people for preventing postherpetic neuralgia (PHN) found no significant difference between placebo and acyclovir. Combining four RCTs, 44.1% of the acyclovir treatment group developed herpetic neuralgia whereas 53.3% of the placebo group developed herpetic neuralgia. Heterogeneity between the four RCTs was moderate: Chi =3.36, df = 2 (P=0.19); I = 40%.

Additionally, there was no significant difference in preventing the incidence of PHN found in the one RCT included in the meta-analysis that compared placebo to PO famciclovir treatment within 72 hours of HZ rash onset. Studies using valaciclovir treatment were not included in the meta-analysis.

PHN was defined as pain at the site of the dermatomic rash at 120 days after the onset of rash, and incidence was evaluated at 1, 4, and 6 months after rash onset.

There was a slight reduction in the incidence of pain at 4 weeks after the onset of rash in the aciclovir group (153 study participants with pain out of 347 study participants in the aciclovir group) versus the placebo group (184 study participants with pain out of 345 study participants in the placebo group). Patients who are prescribed PO antiviral agents after the onset of rash should be informed that their chances of developing PHN are no different than those not taking PO antiviral agents.

A randomized controlled trial found that amitriptyline 25 mg per night for 90 days starting within two days of onset of rash can reduce the incidence of postherpetic neuralgia from 35% to 16% (number needed to treat is 6).

Good oral hygiene (thorough tooth brushing and flossing and regular professional cleaning and examination) may be helpful to prevent these disorders. Drinking plenty of water and the production of enough saliva, aid in the reduction of bacterial growth. Minimizing irritants or injury in the mouth when possible can aid in the prevention of glossitis. Avoiding excessive use of any food or substance that irritates the mouth or tongue may also help.

Treatment includes irrigation and debridement of necrotic areas (areas of dead and/or dying gum tissue), oral hygiene instruction and the uses of mouth rinses and pain medication. If there is systemic involvement, then oral antibiotics may be given, such as metronidazole. As these diseases are often associated with systemic medical issues, proper management of the systemic disorders is appropriate.

Gingivostomatitis (also known as primary herpetic gingivostomatitis or orolabial herpes) is a combination of gingivitis and stomatitis, or an inflammation of the oral mucosa and gingiva. Herpetic gingivostomatitis is often the initial presentation during the first ("primary") herpes simplex infection. It is of greater severity than herpes labialis (cold sores) which is often the subsequent presentations. Primary herpetic gingivostomatitis is the most common viral infection of the mouth.

Primary herpetic gingivostomatitis (PHGS) represents the clinically apparent pattern of primary herpes simplex virus (HSV) infection, since the vast majority of other primary infections are symptomless. PHGS is caused predominantly by HSV-1 and affects mainly children. Prodromal symptoms, such as fever, anorexia, irritability, malaise and headache, may occur in advance of disease. The disease presents as numerous pin-head vesicles, which rupture rapidly to form painful irregular ulcerations covered by yellow–grey membranes. Sub-mandibular lymphadenitis, halitosis and refusal to drink are usual concomitant findings.