Medication is the main method of managing pain in TMD, mostly because there is little if any evidence of the effectiveness of surgical or dental interventions. Many drugs have been used to treat TMD pain, such as analgesics (pain killers), benzodiazepines (e.g. clonazepam, prazepam, diazepam), anticonvulsants (e.g. gabapentin), muscle relaxants (e.g. cyclobenzaprine), and others. Analgesics that have been studied in TMD include non-steroidal anti-inflammatory drugs (e.g. piroxicam, diclofenac, naproxen) and cyclo-oxygenase-2 inhibitors (e.g. celecoxib). Topical methyl salicylate and topical capsaicin have also been used. Other drugs that have been described for use in TMD include glucosamine hydrochloride/chondroitin sulphate and propranolol. Despite many randomized control trials being conducted on these commonly used medications for TMD a systematic review carried out in 2010 concluded that there was insufficient evidence to support or not to support the use of these drugs in TMD. Low-doses of anti-muscarinic tricyclic antidepressants such as amitriptyline, or nortriptyline have also been described. In a subset of people with TMD who are not helped by either noninvasive and invasive treatments, long term use of opiate analgesics has been suggested, although these drugs carry a risk of drug dependence and other side effects. Examples include morphine, fentanyl, oxycodone, tramadol, hydrocodone, and methadone.

Botulinum toxin solution ("Botox") is sometimes used to treat TMD. Injection of botox into the lateral pterygoid muscle has been investigated in multiple randomized control trials, and there is evidence that it is of benefit in TMD. It is theorized that spasm of lateral pterygoid causes anterior disc displacement. Botulinum toxin causes temporary muscular paralysis by inhibiting acetylcholine release at the neuromuscular junction. The effects usually last for a period of months before they wear off. Complications include the creation of a "fixed" expression due to diffusion of the solution and subsequent involvement of the muscles of facial expression, which lasts until the effects of the botox wear off. Injections of local anesthetic, sometimes combined with steroids, into the muscles (e.g. the temoralis muscle or its tendon) are also sometimes used. Local anesthetics may provide temporary pain relief, and steroids inhibit pro-inflammatory cytokines. Steroids and other medications are sometimes injected directly into the joint (See Intra-articular injections).

TMD can be difficult to manage, and since the disorder transcends the boundaries between several health-care disciplines — in particular, dentistry and neurology, the treatment may often involve multiple approaches and be multidisciplinary. Most who are involved in treating and, researching TMD now agree that any treatment carried out should not permanently alter the jaw or teeth, and should be reversible. To avoid permanent change, over-the-counter or prescription pain medications may be prescribed.

The perforation may heal in a few weeks, or may take up to a few months. Some perforations require intervention. This may take the form of a paper patch to promote healing (a simple procedure by an ear, nose and throat specialist), or surgery (tympanoplasty). However, in some cases, the perforation can last several years and will be unable to heal naturally.

Hearing is usually recovered fully, but chronic infection over a long period may lead to permanent hearing loss. Those with more severe ruptures may need to wear an ear plug to prevent water contact with the ear drum.

Perforation of the eardrum leads to conductive hearing loss, which is usually temporary. Other symptoms may include tinnitus, earache or a discharge of mucus.

Certain drugs, including both prescribed and recreational drugs are thought by some to cause the development of bruxism, however others argue that there is insufficient evidence to draw such a conclusion. Examples may include dopamine agonists, dopamine antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors, alcohol, cocaine, and amphetamines (including those taken for medical reasons). In some reported cases where bruxism is thought to have been initiated by selective serotonin reuptake inhibitors, decreasing the dose resolved the side effect. Other sources state that reports of selective serotonin reuptake inhibitors causing bruxism are rare, or only occur with long-term use.

Specific examples include levodopa (when used in the long term, as in Parkinson's disease), fluoxetine, metoclopramide, lithium, cocaine, venlafaxine, citalopram, fluvoxamine, methylenedioxyamphetamine (MDA), methylphenidate (used in attention deficit hyperactive disorder), and gamma-hydroxybutyric acid (GHB) and similar gamma-aminobutyric acid-inducing analogues such as phenibut. Bruxism can also be exacerbated by excessive consumption of caffeine, as in coffee, tea or chocolate. Bruxism has also been reported to occur commonly comorbid with drug addiction. Methylenedioxymethamphetamine (MDMA, ecstasy) has been reported to be associated with bruxism, which occurs immediately after taking the drug and for several days afterwards. Tooth wear in people who take ecstasy is also frequently much more severe than in people with bruxism not associated with ecstasy.

Many different medications have been used to treat bruxism, including benzodiazepines, anticonvulsants, beta blockers, dopamine agents, antidepressants, muscle relaxants, and others. However, there is little, if any, evidence for their respective and comparative efficacies with each other and when compared to a placebo. A systematic review is underway to investigate the evidence for drug treatments in sleep bruxism.

Specific drugs that have been studied in sleep bruxism are clonazepam, levodopa, amitriptyline, bromocriptine, pergolide, clonidine, propranolol, and l-tryptophan, with some showing no effect and others appear to have promising initial results; however, it has been suggested that further safety testing is required before any evidence-based clinical recommendations can be made. When bruxism is related to the use of selective serotonin reuptake inhibitors in depression, adding buspirone has been reported to resolve the side effect. Tricyclic antidepressants have also been suggested to be preferable to selective serotonin reuptake inhibitors in people with bruxism, and may help with the pain.

A number of endoscopic devices have been tested to treat chronic heartburn.

- Endocinch, puts stitches in the lower esophogeal sphincter (LES) to create small pleats to help strengthen the muscle. However, long-term results were disappointing, and the device is no longer sold by Bard.

- Stretta procedure, uses electrodes to apply radio-frequency energy to the LES. A 2015 systematic review and meta-analysis in response to the systematic review (no meta-analysis) conducted by SAGES did not support the claims that Stretta was an effective treatment for GERD. A 2012 systematic review found that it improves GERD symptoms.

- NDO Surgical Plicator creates a plication, or fold, of tissue near the gastroesophageal junction, and fixates the plication with a suture-based implant. The company ceased operations in mid-2008, and the device is no longer on the market.

- Transoral incisionless fundoplication, which uses a device called Esophyx, may be effective.

Immunotherapy with immune checkpoint inhibitors is being investigated in head and neck cancers.

Specific treatment depends on the location, type, and stage of the tumour. Treatment may involve surgery, radiotherapy, or chemotherapy, alone or in combination. This is a specialised area which requires the coordinated expertise of ear, nose and throat (ENT) surgeons (Otorhinolaryngologists) and Oncologists. A severely affected patient may require a laryngectomy, the complete or partial removal of the vocal cords.

Certain foods and lifestyle are considered to promote gastroesophageal reflux, but most dietary interventions have little supporting evidence. Avoidance of specific foods and of eating before lying down should be recommended only to those in which they are associated with the symptoms. Foods that have been implicated include coffee, alcohol, chocolate, fatty foods, acidic foods, and spicy foods. Weight loss and elevating the head of the bed are generally useful. A wedge pillow that elevates the head may inhibit gastroesophageal reflux during sleep. Stopping smoking and not drinking alcohol do not appear to result in significant improvement in symptoms. Although moderate exercise may improve symptoms in people with GERD, vigorous exercise may worsen them.

Around 75% of cases are caused by alcohol and tobacco use.

Tobacco smoke is one of the main risk factors for head and neck cancer and one of the most carcinogenic compounds in tobacco smoke is acrylonitrile. (See Tobacco smoking). Acrylonitrile appears to indirectly cause DNA damage by increasing oxidative stress, leading to increased levels of 8-oxo-2'-deoxyguanosine (8-oxo-dG) and formamidopyrimidine in DNA (see image). Both 8-oxo-dG and formamidopyrimidine are mutagenic. DNA glycosylase NEIL1 prevents mutagenesis by 8-oxo-dG and removes formamidopyrimidines from DNA.

However, cigarette smokers have a lifetime increased risk for head and neck cancers that is 5- to 25-fold increased over the general population.

The ex-smoker's risk for squamous cell cancer of the head and neck begins to approach the risk in the general population twenty years after smoking cessation. The high prevalence of tobacco and alcohol use worldwide and the high association of these cancers with these substances makes them ideal targets for enhanced cancer prevention.

Smokeless tobacco is cause of oral and pharyngeal cancers (oropharyngeal cancer). Cigar smoking is an important risk factor for oral cancers as well.

Other environmental carcinogens suspected of being potential causes of head and neck cancer include occupational exposures such as nickel refining, exposure to textile fibers, and woodworking. Use of marijuana, especially while younger, is linked to an increase in squamous-cell carcinoma cases while other studies suggest use is not shown to be associated with oral squamous cell carcinoma, or associated with decreased squamous cell carcinoma.

Incidence is five in 100,000 (12,500 new cases per year) in the USA. The American Cancer Society estimated that 9,510 men and women (7,700 men and 1,810 women) would be diagnosed with and 3,740 men and women would die of laryngeal cancer in 2006.

Laryngeal cancer is listed as a "rare disease" by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH). This means that laryngeal cancer affects fewer than 200,000 people in the U.S.

The primary method of prevention for pertussis is vaccination. Evidence is insufficient to determine the effectiveness of antibiotics in those who have been exposed, but are without symptoms. Preventive antibiotics, however, are still frequently used in those who have been exposed and are at high risk of severe disease (such as infants).

The antibiotics erythromycin, clarithromycin, or azithromycin are typically the recommended treatment. Newer macrolides are frequently recommended due to lower rates of side effects. Trimethoprim-sulfamethoxazole (TMP/SMX) may be used in those with allergies to first-line agents or in infants who have a risk of pyloric stenosis from macrolides.

A reasonable guideline is to treat people age >1 year within 3 weeks of cough onset and infants age <1 year and pregnant women within 6 weeks of cough onset. If the person is diagnosed late, antibiotics will not alter the course of the illness, and even without antibiotics, they should no longer be spreading pertussis. Antibiotics when used early decrease the duration of infectiousness, and thus prevent spread. Short-term antibiotics (azithromycin for 3–5 days) are as effective as long-term treatment (erythromycin 10–14 days) in eliminating "B. pertussis" with fewer and less severe side effects.

People with pertussis are infectious from the beginning of the catarrhal stage (a runny nose, sneezing, low-grade fever, symptoms of the common cold) through the third week after the onset of paroxysms (multiple, rapid coughs) or until 5 days after the start of effective antimicrobial treatment.

Effective treatments of the cough associated with this condition have not been developed.