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Oesophageal Strictures

Management Team

Oesophageal Strictures

Overview

Types of oesophageal strictures. EoE, Eosinophilic esophagitis

Oesophageal strictures refer to the narrowing or tightening of the oesophagus, which can cause difficulty swallowing (dysphagia), regurgitation, and discomfort. These strictures are caused by varied factors, including inflammatory, neoplastic, traumatic, and congenital factors. The narrowing can be partial or complete, and the degree of severity can vary. Oesophageal strictures can develop over time and lead to progressive difficulty in swallowing.

Strictures can be broadly classified based on their aetiology (underlying cause) and the mechanisms involved in their formation.

  • Benign oesophageal strictures: These are non-cancerous strictures caused by chronic injury, inflammation, or scarring of the oesophageal lining.
    • Corrosive strictures
    • Radiation-induced strictures
    • Eosinophilic esophagitis (EoE) strictures
    • Post-surgical strictures
    • Achalasia-related strictures
  • Peptic (gastroesophageal reflux disease - GERD) strictures
  • Malignant oesophageal strictures: These strictures occur due to oesophageal cancer or metastatic cancer that involves the oesophagus.
  • Congenital oesophageal strictures: These strictures are present at birth and are relatively rare.
  • Congenital oesophageal atresia with strictures

TypeCauseRegion affectedSymptoms
Peptic (GERD) strictureChronic acid reflux causing fibrosisDistal oesophagus (near LES)Dysphagia, heartburn, regurgitation
Corrosive strictureIngestion of caustic substances (acids or alkalis)Middle to distal oesophagusImmediate pain, dysphagia, aspiration
Radiation-induced strictureRadiation therapy for cancersMiddle to distal oesophagusDysphagia, chest pain
Eosinophilic esophagitis (EoE) strictureChronic allergic inflammationProximal to mid-oesophagusDysphagia, food impaction
Post-surgical strictureScarring after surgery (e.g., fundoplication, esophagectomy)Near the site of surgeryDysphagia, regurgitation
Achalasia-related strictureDysfunctional motility in achalasiaDiffuse, often at LES*Progressive dysphagia, regurgitation
Metastatic strictureSpread from primary cancersAny part of the oesophagusDysphagia, weight loss, regurgitation
Congenital strictureAbnormal foetal development (atresia, webs)Upper oesophagusFeeding difficulties, aspiration (in neonates)

*LES, Lower oesophageal sphincter

  • Gastroesophageal reflux disease (Peptic Stricture)
  • Eosinophilic oesophagitis: An allergic condition where eosinophils (a type of white blood cell) infiltrate the oesophagus, leading to inflammation and fibrosis. (EoE stricture)
  • Radiation therapy
  • Achalasia
  • Corrosion-related oesophageal injury: Injuries caused by swallowing corrosive substances, like acids or alkalis, can result in strictures. (Corrosive stricture)
  • Infections: Certain infections (like candida or herpes) may cause oesophageal damage, leading to stricture formation.
  • Surgical complications (Post-surgical stricture)
  • Oesophageal cancer (Malignant stricture)
  • Hiatal hernia
  • Peptic ulcers
  • Foreign body ingestion
  • Congenital issues
  • Plummer-Vinsion syndrome
  • Family history of allergies or asthma
  • Age

  • Dysphagia (difficulty swallowing)
  • Odynophagia (painful swallowing
  • Regurgitation
  • Weight loss
  • Heartburn
  • Coughing or choking
  • Persistent hiccups

  • Upper endoscopy (esophagogastroduodenoscopy, EGD): This is the most definitive diagnostic tool for oesophageal strictures. During EGD, a camera bound to a fine tube is guided into the oesophagus through the mouth to confirm or negate the presence of a stricture and take biopsies if needed. Endoscopy also helps assess the degree of damage (inflammation, ulceration, and scarring).
  • Barium swallow (X-ray): A contrast study where the patient swallows a barium solution, allowing radiologists to see the contours of the oesophagus and identify any narrowing or blockages. This technique can show the location and extent of the stricture, and is useful for assessing motility
  • Oesophageal manometry: This test measures the pressure and muscle function and motility of the oesophagus and lower oesophageal sphincter.
  • CT or MRI: These imaging modalities can determine stricture position and severity, and rule out other causes, such as tumours.

  • Endoscopic treatment: This is generally performed for established strictures.
    • Endoscopic balloon dilation: One of the primary treatments for oesophageal strictures is endoscopic dilation, where a balloon is inflated to stretch the narrowed part of the oesophagus.
    • Laser therapy: It may be used for treating strictures, particularly if the narrowing is severe or resistant to dilation.
    • Oesophageal stenting: If dilation is ineffective or the stricture recurs frequently, a stent might be inserted to keep the oesophagus open. This is usually considered a temporary or adjunctive solution.
  • Neutralisation: In case of corrosive strictures, or strictures caused by ingestion of a chemical, neutralisation of the chemical immediately after consumption is an effective management strategy.
  • Medications:
    • Proton pump inhibitors (PPIs): If the stricture is caused by GERD, PPIs can reduce acid production, decreasing further damage to the oesophagus.
    • H2-receptor antagonists: Similar to PIPs, these antagonists also decrease stomach acid production; however, these are less effective.
    • Antacids: These can provide temporary relief for heartburn symptoms.
    • Corticosteroids: For eosinophilic oesophagitis, corticosteroids can reduce inflammation and prevent further scarring.
    • Antibiotics or antifungals: If an infection (such as Candida) is the cause, appropriate antimicrobial therapy will be needed.
  • Surgical intervention: In severe cases or when dilation fails, surgery may be required. This could involve cutting away the affected portion or creating a bypass.
  • Dietary modifications: Patients are often advised to avoid foods that might irritate the oesophagus, particularly acidic or spicy foods. Depending on stricture severity, a soft food diet or liquid diet might be recommended.
  • Management of underlying conditions: Treating the underlying cause, such as controlling GERD, managing eosinophilic oesophagitis, or treating achalasia, is crucial for preventing recurrence of strictures.
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Benign Prostate Enlargement or Hyperplasia (BPE or BPH)

Management Team

Benign Prostate Enlargement or Hyperplasia (BPE or BPH)

Overview

This is a common, non-cancerous condition that may occur as a patient grows older. It is characterised by an enlargement of the prostate and is typically accompanied by urinary discomfort.

The symptoms of BPE/H are as follows:

  • Increased frequency of urination
  • Bladder urgency, which is a strong, sudden need to urinate
  • Nocturia, increased frequency of urination at night
  • Poor urinary flow
  • Straining during urination
  • Stopping and starting during urination or an intermittent urine stream
  • Feeling of incomplete urination
  • Burning sensation during urination, accompanied by fever or chills
  • Bladder stones

BPE can be diagnosed via the following investigations:

  • Digital rectal examination: A healthcare professional will manually palpitate the area around the prostrate and assess its status
  • Ultrasound KUB: An ultrasound examination of the kidneys, ureters, and bladder
  • Uroflowmetry: A test that measures the speed, amount, and duration of urination
  • Serum PSA: A blood test that checks for a protein produced by the prostate gland
  • Urinalysis: A common urine test

The following treatments are available for BPE:

  • Transurethral resection of the prostate (TURP): This surgical procedure involves removing a portion of the prostate gland. We offer both monopolar and bipolar TURP
  • Laser enucleation (LEP): A pulsed laser beam is used to remove tissue from within the prostate. It is a minimally invasive procedure. We offer LEP using two types of lasers (HoLEP and ThuLEP)
  • Laser vaporisation: A high-power green light laser is used to remove tissue from the prostate gland
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Oesophageal Cancer

Management Team

Oesophageal Cancer

Overview

Oesophageal cancer refers to a cancerous tissue (tumour) that has its origins in the lining of the oesophagus but can spread deeper and upwards or downwards along the food pipe. This rare entity is often diagnosed at an advanced stage as patients do not realise that they are affected until the tumour is big and obstructs the oesophageal lumen.

Oesophageal cancers are of the following three types:

  • Adenocarcinomas: They originate from glandular cells, which are located in the lower part of the food pipe, i.e., near the stomach.
  • Squamous cell carcinomas: They originate from the squamous cells that line the upper and middle parts of the food pipe.
  • Other rare types of oesophageal cancers: Though most oesophageal cancers are adenosarcomas or squamous cell sarcomas, other rarer types exist.
    • Small cell cancers: The origins of this cancer are not clear.
    • Soft tissue sarcomas: These originate from cells of tissues that support and protect organs.
    • Poorly differentiated neuroendocrine cancers: These originate from cells of the neuroendocrine system.

  • Gastroesophageal reflux disease (GERD)
  • Acid reflux
  • Obesity and overweight
  • Smoking and drinking
  • Vegetable & fruit-poor diets
  • Age
  • Achalasia
  • Chronic irritation or injury to the oesophagus

Oesophageal cancer may be asymptomatic (no noticeable symptoms) initially; however, with disease progression, symptoms may appear. These symptoms include:

  • Dysphagia (difficulty swallowing
  • Unexplained weight loss
  • Chest pain
  • Regurgitation of food
  • Hoarseness
  • Chronic cough
  • Indigestion or heartburn
  • Vomiting or coughing up blood (in more advanced stages)

  • Endoscopy: This method involves visualising the interior of the oesophagus and possibly suspicious using a camera attached to a very fine, flexible tube.
  • Endoscopic ultrasound: This technique helps determine tumour size and evaluate tumour metastasis, i.e., spread to nearby tissues or lymph nodes.
  • Imaging tests: CT, MRI, or PET are used to assess cancer spread (metastasis).
  • Biopsy: This technique is used to detect cancer cells in the oesophageal tissue.

  • Surgical approach: In some cases, removing the tumour through surgery is an option. This may involve partial or total removal of the oesophagus (esophagectomy).
  • Endoscopic therapy: For early-stage cancers, techniques like laser therapy or photodynamic therapy may be used to eliminate cancer cells.
  • Radiation therapy: This modality involving high-energy irradiation either alone or in conjunction with chemotherapy can be used to target and kill abnormally growing cells (tumour cells).
  • Chemotherapy: This modality generally used in combination with other treatments eliminates cancer cells and restricts their growth.
  • Targeted therapy: This strategy involves using drugs e.g., trastuzumab (HER2 inhibitor), bevacizumab (VEGF inhibitor), and EGFR inhibitors that target key molecules driving cancer cell growth and survival. It offers new options for managing advanced or metastatic disease.
  • Immunotherapy: Checkpoint inhibitors like pembrolizumab and nivolumab have emerged as important treatment options for individuals with advanced oesophageal cancer, especially those with high PD-L1 expression.

Consult a medical professional if you have difficulty swallowing, unexplained weight loss, or other persistent symptoms like long-standing acidity and heartburn.

  • Avoiding smoking and excessive alcohol use.
  • Maintaining optimal weight and having a balanced diet.
  • Orderly screening of high-risk individuals, especially those having chronic GERD or a history of oesophageal conditions.
  • Managing GERD symptoms and Barrett’s oesophagus (if present).
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Oesophageal Dysmotility due to Gastroesophageal Reflux Disease (GERD)

Management Team

Oesophageal Dysmotility due to Gastroesophageal Reflux Disease (GERD)

Overview

GERD can lead to oesophageal motility dysfunction owing to improper closing of the lower oesophageal sphincter (LES) and subsequent stomach acid to reflux into the oesophagus.

Chronic acid exposure due to GERD: GERD can lead to hypotension of the LES (a condition where the LES does not maintain the pressure required to prevent the backflow of the stomach contents into the oesophagus) as well as impaired oesophageal peristalsis, often due to chronic acid exposure.

  • Heartburn
  • Regurgitation
  • Chest pain
  • Dysphagia
  • Sensation of a lump in the throat

  • Oesophageal manometry: This condition may manifest as reduced peristalsis and LES dysfunction in oesophageal manometry.
  • 24-hour pH monitoring: This is often employed to confirm acid reflux.

  • Medications:
    • Antacids, PPIs, and H2 receptor antagonists: These may be used to reduce acid production.
    • Prokinetic agents: These agents (e.g., metoclopramide and domperidone) may be used to improve oesophageal motility.
  • Fundoplication surgery: In some cases, fundoplication surgery to repair the LES may be considered.
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O

Scleroderma Oesophagus

Management Team

Scleroderma Oesophagus

Overview

Scleroderma can cause hardening and thickening of the internal organs, including the oesophagus. In scleroderma, the smooth muscles of the oesophagus become weakened, leading to impaired peristalsis.

  • Immune dysregulation: This is the primary cause of scleroderma as it is an autoimmune disease, wherein the autoimmune reaction results in oesophageal fibrosis (scarring).
  • Atrophy of oesophageal smooth muscles: In scleroderma, the smooth muscle fibres of the oesophagus undergo atrophy and fibrosis, impairing the ability of the oesophagus to contract effectively. This leads to a loss of normal peristalsis (the coordinated wave-like contractions that move food down the oesophagus).
  • Decreased lower oesophageal sphincter (LES) tone: One of the most significant features of scleroderma oesophagus is a reduction in LES pressure. This can lead to gastroesophageal reflux disease (GERD), as the weakened LES cannot effectively prevent stomach contents from refluxing into the oesophagus. This is often exacerbated by the loss of oesophageal motility.
  • Neuropathy (nerve problem that causes pain): The vagus nerve (which controls oesophageal motility) can be affected by the autoimmune reaction, leading to neuropathy or damage to the neural pathways that control smooth muscle contraction and relaxation. This results in the loss of coordination between muscle layers, leading to disordered motility. This can cause a phenomenon called "hypomotility", where the oesophagus has decreased or absent peristalsis, or "aperistalsis", where the normal peristaltic waves are either absent or ineffective.

  • Dysphagia (difficulty swallowing)
  • Heartburn (burning sensation in the upper abdomen)
  • Regurgitation
  • Acid reflux (backflow of stomach acid into the oesophagus)
  • Aspiration can occur in severe cases, i.e., food or liquid can be aspirated into the lungs due to the dysfunction of the swallowing mechanism, which can lead to aspiration pneumonia.

  • Oesophageal manometry: In this test, scleroderma oesophagus may manifest as reduced peristalsis and lower oesophageal sphincter (LES) relaxation.
  • Barium swallow: In this test, the LES may exhibit a bird-beak appearance.

Treatment modalities for scleroderma oesophagus include:

  • Medications:
    • Proton pump inhibitors and H2 receptor blockers: These are used to manage acid reflux.
    • Prokinetic agents: Agents like metoclopramide and domperidone are used to improve oesophageal motility.
  • Stricture dilation: In some cases, stricture dilation may be performed to reduce the pressure on the oesophagus.
  • Oesophageal surgery: This may be necessary in some cases.
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S

Nutcracker Oesophagus

Management Team

Nutcracker Oesophagus

Overview

This condition also known as hypercontractile oesophagus or jackhammer oesophagus is characterised by excessively strong (and prolonged) oesophageal contractions, resulting in pain and dysphagia (difficulty swallowing). The contractions may be normal in frequency but are excessively forceful.

  • Neuromuscular dysfunction: Disrupted neural regulation of the oesophagus, including impaired inhibitory neurotransmission, may lead to hypercontractility.
  • Chronic acid reflux
  • Psychological stress
  • Oesophageal inflammation: Conditions like eosinophilic esophagitis or general esophagitis may disrupt normal motility.
  • Genetic predisposition
  • Gastroesophageal reflux disease (GERD)
  • Ageing
  • Dietary triggers: Certain foods and drinks, especially those that are spicy or acidic, may trigger or worsen symptoms.

  • Dysphagia (difficulty swallowing)
  • Intense chest pain that is occasionally confused with a heart attack
  • Sensation of food getting stuck in the throat
  • Heartburn (burning sensation in the chest)

  • Oesophageal manometry: This is the primary diagnostic modality for nutcracker oesophagus. Diagnosis is based on the detection of hypercontractile contractions.
  • Oesophageal high-resolution manometry (HRM): This is a more advanced form of manometry. It can provide a more detailed, topographic map of pressure changes in the oesophagus and may be particularly helpful in differentiating nutcracker oesophagus from other oesophageal motility disorders.
  • Endoscopy: It is typically normal in nutcracker oesophagus and is performed to exclude other structural or inflammatory causes (e.g., tumours, strictures, or GERD-related esophagitis).

  • Medications: Various medications are used to relax the oesophagus
    • Calcium channel blockers
    • Nitrates
    • Botulinum toxin injections
    • Prokinetic medications (e.g., metoclopramide, domperidone)
    • Antidepressants (to regulate oesophageal nerve activity)
  • Surgical myotomy: In some cases, myotomy (a procedure involving trimming the circular fibres of the lower oesophageal sphincter (LES) to facilitate movement of food along the food pipe may be considered (if conservative measures fail).
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N

Diffuse Oesophageal Spasm (DES)

Management Team

Diffuse Oesophageal Spasm (DES)

Overview

DES is characterised by uncoordinated, often very strong, and irregular oesophageal contractions. These spasms can result in substantial chest pain and dysphagia (difficulty swallowing).

The cause of DES is unclear, but the following may play a role in its occurrence:

  • Neuromuscular dysfunction:
    • Impaired inhibitory neurotransmission: Normally, the oesophagus uses excitatory as well as inhibitory neurotransmitters to regulate smooth muscle contraction. In DES, there may be reduced or absent inhibitory signals from the nerves that control digestion and related processes (enteric system), leading to simultaneous uncoordinated contractions of the oesophageal muscles.
    • Disrupted smooth muscle function: The smooth muscle in the oesophagus may respond abnormally to neural signals, causing spasms or contractions that are out of sync with normal peristalsis.
  • Gastroesophageal reflux disease (GERD)
  • Hypersensitivity to acid
  • Psychological stress
  • Oesophageal inflammation
  • Genetic factors
  • Ageing
  • Oesophageal structural abnormalities

  • Chest pain (which may mimic heart attack symptoms)
  • Dysphagia (difficulty swallowing)
  • Regurgitation (this is less common than in other oesophageal motility disorders)

  • Oesophageal manometry: This test is used to diagnose DES based on the measurement of uncoordinated contractions.
  • Barium swallow: A barium swallow may reveal a "corkscrew" pattern in the oesophagus.

  • Medications:
    • Calcium channel blockers or nitrates: These are used to relax the oesophageal smooth muscles and reduce the spasms.
    • Prokinetic agents and antidepressants: These are used for nerve modulation.
  • Botulinum toxin (Botox): In refractory (nonresponding) cases, Botox injections may be considered to reduce spasms by inhibiting the release of acetylcholine, which is known to induce smooth muscle contraction.
  • Surgery: This is used in severe cases.
    • Esophagectomy (removal of all or parts of the oesophagus)
    • Myotomy (cutting of muscles in the oesophagus)
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D

Achalasia Cardia

Management Team

Achalasia Cardia

Overview

Achalasia cardia is a serious disorder affecting the food pipe (oesophagus). It is a rare condition, wherein the lower oesophageal sphincter (LES) is unable to relax properly, a phenomenon that hinders the efficient passage of food and liquids into the stomach. Furthermore, peristalsis (the coordinated contractions of the oesophagus) is also affected, which further impairs the movement of food. This leads to dysphagia (difficulty swallowing), regurgitation, and other symptoms related to poor oesophageal motility.

  • Neurological dysfunction: The primary cause of achalasia cardia is the degeneration of specialised nerve cells (ganglion cells) that are responsible for controlling the muscles of the oesophagus and the LES. Without proper nerve function, the LES fails to relax, and the oesophagus loses its ability to move food downward via peristalsis.
  • Genetic factors
  • Autoimmune responses
  • Viral infections: Certain viral infections, particularly Chagas disease (caused by Trypanosoma cruzi), can lead to achalasia by damaging the nerves in the oesophagus.
  • Other diseases: Achalasia can also occur secondary to other diseases, such as Chagas disease or cancer of the oesophagus, although this is much less common.

  • Difficulty in swallowing): even swallowing liquids may become difficult as the disease progresses.
  • Regurgitation of food or liquids, especially when reclining. This might result in coughing or choking, and can sometimes even culminate in aspiration (food or liquid entering the lungs).
  • Aspiration pneumonia
  • Heartburn
  • Chest pain
  • Weight loss

  • Barium swallow (Esophagram): This imaging modality involves swallowing a contrast medium (barium) by the patient to visualise the oesophagus. In the barium swallow test, achalasia typically presents a "bird's beak" appearance at the lower oesophageal sphincter (LES), where the oesophagus narrows down owing to the inability of the LES to relax.
  • Oesophageal manometry: This test is the gold standard for diagnosing achalasia; it involves measuring the pressure inside the oesophagus and evaluating the function of the LES. In achalasia, the manometry will reveal a lack of oesophageal peristalsis and incomplete LES relaxation during swallowing.
  • Endoscopy (oesophagogastroduodenoscopy or EGD)
  • Oesophageal pH monitoring: This test involves evaluating the amount of acid reflux into the oesophagus. It is useful to rule out gastroesophageal reflux disease (GERD) or other reflux-related conditions.
  • CT or MRI

  • Medications:
    • Nitrates or calcium channel blockers: These medications may help relax the lower oesophageal stricture (LES) and improve swallowing. However, their effectiveness is usually limited, and they are often only helpful in mild cases or as a short-term solution(s).
    • Botulinum toxin (Botox): Injections of Botox into the LES can temporarily paralyse the muscle, allowing it to relax and improve swallowing. This treatment is often used in older patients or individuals who are not candidates for surgery, but the effects typically wear off after a few months.
  • Pneumatic dilation: This involves using a balloon to stretch and widen the LES. The procedure is performed under sedation and can offer significant symptom relief in many patients. It is effective for many, but the procedure may need to be repeated, and there is a risk of oesophageal perforation.
  • Surgical treatment:
    • Heller myotomy: This surgical modality involves cutting the muscle of the LES to allow easier passage of food into the stomach. Heller myotomy is a very effective treatment for achalasia and is typically performed laparoscopically (minimally invasive surgery that involves making tiny incisions).
    • Peroral endoscopic myotomy (POEM): This endoscopic procedure (less invasive than Heller myotomy) involves the use of an endoscope to cut the muscle of the LES. POEM is more effective and less invasive than Heller myotomy.
    • Oesophageal stenting: In rare cases, a stent may be placed in the oesophagus to keep it open. This is typically used when other treatments are not effective or if there is a significant narrowing.
  • Lifestyle and dietary changes:
    • Eating smaller portions and consuming soft, easy-to-swallow foods may help manage symptoms.
    • Avoiding lying down immediately after eating and eating slowly may also alleviate regurgitation and discomfort.

Consult a medical professional if you experience dysphagia (difficulty swallowing), chest pain, regurgitation, or unintentional weight loss.

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A

Leukoplakia

Management Team

Leukoplakia

Overview

Leukoplakia refers to the growth of white patches or plaques that develop on the mucous membranes inside the oral cavity, including the tongue, cheeks, and gums. The patches are often thickened, and they typically cannot be wiped off, a feature that distinguishes them from other types of white lesions in the mouth, such as those caused by oral thrush. Leukoplakia is considered a precancerous condition as leukoplakia lesions have the potential to develop into oral cancer; however, not all lesions become cancerous.

  • Tobacco use: Smoking (even smokeless tobacco) is the most well-known risk factor for leukoplakia. Constant irritation caused by tobacco products can lead to the formation of these white patches.
  • Alcohol consumption: Heavy drinking, especially in combination with tobacco use, increases the risk of leukoplakia and may also increase the risk of malignant transformation.
  • Chronic irritation or trauma: Regular irritation from ill-fitting dentures, sharp edges of teeth, or other mechanical factors can contribute to the development of leukoplakia.
  • Human papillomavirus (HPV): Some studies suggest that certain strains of the human papillomavirus (HPV), especially HPV-16, may be involved in leukoplakia development, particularly in the context of oral cancers.
  • Weakened immune system: Conditions like HIV/AIDS or immunosuppressive treatments (e.g., chemotherapy, organ transplant drugs) can increase susceptibility to leukoplakia.
  • Nutritional deficiencies: Deficiencies of vitamins, particularly vitamin A and B12, may contribute to leukoplakia.
  • Age and gender: Leukoplakia is more common in the elderly or middle-aged individuals. Further, men are at a higher risk of being affected by this condition than women.
  • Other factors: Certain chronic conditions, such as lichen planus (a disease that affects the skin and mucous membranes), can also predispose individuals to leukoplakia.

  • White patches: The hallmark of leukoplakia is the appearance of thick, white or greyish patches in the mouth. These patches may be slightly raised or flat and cannot be wiped away.
  • Rough texture: These patches are often thick and rough in texture. They may be irregular in shape.
  • Burning sensation: Though most people with leukoplakia do not experience pain or other symptoms, some individuals may feel a burning sensation or discomfort.
  • Ulceration: In some cases, leukoplakia patches may appear red, ulcerated, or indurated (hardened), which may suggest dysplasia (abnormal cell growth) or early stages of cancer.

  • Visual examination: The mouth and the lesions are visually inspected to look for signs, such as changes in texture, size, or colour, which may indicate more severe issues.
  • Biopsy: This may be recommended for persistent or suspicious lesions to determine whether the lesion/patch is dysplastic (associated with abnormal cell growth) or cancerous.
  • Other tests: Depending on the clinical presentation, i.e., the features and duration of lesion presentation, additional tests (e.g., imaging or HPV testing) may be recommended.

Treatment for leukoplakia is usually focused on addressing the underlying causes, managing symptoms, and monitoring the condition for signs of malignant transformation.

  • Eliminating irritation:
    • Abstinence from smoking and alcohol: One of the most important steps is to quit tobacco use and reduce alcohol consumption, as both are major risk factors for leukoplakia and oral cancer.
    • Address chronic irritation: If ill-fitting dentures, rough dental fillings, or sharp teeth are causing the irritation, they should be adjusted or repaired.
  • Surgical treatment:
    • Surgical removal of lesions: In some cases, particularly if the leukoplakia lesions are large, persistent, or show signs of dysplasia, surgical removal may be necessary.
  • Medications:
    • Topical steroids: In cases where there is significant inflammation or discomfort, topical steroids (like corticosteroid ointments) may be prescribed to reduce irritation and inflammation.
  • Cryotherapy: This technique can be used to remove the patches; it involves freezing the leukoplakia lesion(s) with liquid nitrogen.
  • Laser treatment: Lasers can be used to remove the patches or reduce the size of the lesions, especially in cases of localised leukoplakia.
  • Nutrient supplementation: If leukoplakia is linked to a deficiency (e.g., vitamin A or B12), nutritional supplementation may be recommended.

Consult a healthcare professional, preferably a dentist if you notice any white patches, unusual growth(s), or persistent sores in your mouth.

  • Quit smoking and tobacco use: This is most effective for reducing leukoplakia risk.
  • Limiting alcohol consumption: This can also decrease the risk of leukoplakia, especially when combined with cessation of smoking.
  • Regular dental checkups: These can help detect early signs of leukoplakia and other oral conditions.
  • Healthy diet: This may help decrease leukoplakia risk, particularly if nutritional deficiencies are a contributing factor.
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L

Recurrent Mouth Ulcers

Management Team

Recurrent Mouth Ulcers

Overview

Recurrent mouth ulcers are tiny sores that occur within the oral cavity (mouth), and as the name suggests, they tend to reoccur, i.e., occur periodically. They are also known as canker sores or aphthous ulcers, and maybe painful or result in discomfort. Generally, these ulcers occur on the lips, gums, underside of the tongue, or inner cheeks, and in some individuals these ulcers may become a chronic issue.

  • Minor ulcers (small, heal without scarring)
  • Major ulcers (larger, deeper, may leave scars)
  • Herpetiform ulcers (small clusters of ulcers)

  • Immune system dysregulation: This might result in the erroneous targeting of the cells lining the oral cavity (mouth).
  • Genetic factors
  • Injury: Rough brushing, dental braces, or biting the inside of the cheek can trigger an ulcer.
  • Hormonal changes
  • Nutritional deficiencies: Insufficient iron, zinc, folic acid, or vitamin B12 levels can result in the development of recurrent ulcers.
  • Emotional stress
  • Food sensitivities: Certain foods, such as acidic fruits (e.g., oranges, tomatoes), spicy foods, chocolate, or coffee, may trigger or aggravate ulcers in some individuals.
  • Underlying health conditions: Conditions like celiac disease, HIV/AIDS, and autoimmune diseases can cause or exacerbate recurrent mouth ulcers.
  • Medications: Certain medications, e.g., beta-blockers and NSAIDs like aspirin (and some antibiotics) may trigger mouth ulcers.

  • Painful red sores: Usually round/oval sores with white/yellowish centres and red borders are observed.
  • Soreness: The ulcer may make eating, drinking, and talking painful.
  • Swelling: The ulcer may cause swelling in the affected area.
  • Recurrence: These sores tend to come back after subsiding.

  • Physical examination: A thorough examination of the mouth and affected areas is performed to investigate the appearance, size, and location of the ulcers.
  • Exclusion of other conditions:
    • Laboratory tests: Blood or allergy tests may be performed to exclude infections, nutrient insufficiency, or other underlying conditions, such as HIV/AIDS or celiac disease.
    • Biopsy: If the ulcers are unusually large, persistent, or have atypical (unusual features), a biopsy may be recommended to rule out more serious conditions, like oral cancer or other mucosal diseases.
    • Immunological tests: In cases where autoimmune or inflammatory conditions are suspected (e.g., Behçet’s disease), additional tests might be performed to check for specific markers.

Recurring ulcers of the mouth can be treated and managed using both medical and homemade concoctions. A few treatment strategies have been enumerated below.

  • Topical medications:
    • Hydrocortisone: Topical corticosteroid creams can reduce inflammation and pain.
    • Benzocaine: An over-the-counter topical anaesthetic (such as Orajel) can numb the area to relieve pain.
  • Over-the-counter remedies:
    • Saltwater rinse
    • Antiseptic mouthwashes
    • Aloe vera gels
    • Baking soda paste.
  • Prescription treatments: In cases of frequent and severe ulcers, oral medications, such as colchicine, tetracycline, or other immunosuppressive drugs, may be recommended.
  • Nutritional supplements: If a nutritional deficiency is identified, supplements (iron, vitamin B12, folate, or zinc) may help prevent recurrence.
  • Avoiding triggers: Identifying and avoiding specific triggers (e.g., certain foods, stress, or injury) can reduce the frequency of ulcer occurrence.

  • The ulcers are unusually large, persistent, or painful.
  • In addition to ulcers, you have other symptoms, such as fever or swollen lymph nodes.
  • You experience ulcers frequently (more than three times a year).
  • You have difficulty eating or drinking due to pain.
  • The ulcers don’t heal within 2 weeks.

  • Preventing oral trauma: Using a soft-bristled toothbrush for brushing teeth may prevent trauma to the inside of the mouth.
  • Dietary adjustments: Avoiding foods that trigger ulcers or are acidic and ensuring that one is getting adequate vitamins and minerals can help prevent ulcer occurrence.
  • Protective mouth guards: If you have dental braces, a mouth guard can help reduce irritation that can subsequently cause ulcers.
  • Stress management: Techniques like meditation or yoga that help relieve stress can help prevent ulcer occurrence.
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