Odontogenic Sinusitis: Classification, Etiology, Clinical Presentation, Diagnosis, and Treatment
A detailed overview of odontogenic maxillary sinusitis: causes, symptoms of acute and chronic inflammation, diagnosis, and modern treatment approaches.
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Chronic laryngitis belongs to a group of persistent inflammatory laryngeal conditions lasting longer than 3 weeks (primarily develops due to prolonged exposure to various irritants). Forms of the disease vary by etiology (cause) and the nature of pathomorphological changes in the mucosa — ranging from catarrhal inflammation to hyperplasia or atrophy. The precise identification of the form defines the treatment strategy and prognosis.
The primary clinical, morphological, and etiological forms of chronic laryngitis include:
The most common causes of chronic catarrhal laryngitis are smoking, excessive vocal strain, and allergens. The inflammatory process may spread from the nasopharynx or oropharynx, or from the lower respiratory tract. Recurrent sinusitis, rhinitis, tracheitis, and bronchitis may contribute to chronic laryngitis.
In patients with chronic laryngitis, the following bacteria are present: Staphylococcus aureus, Haemophilus influenzae, Candida albicans, Moraxella nonliquefaciens, Neisseria meningitidis, Streptococcus pneumoniae, Lactobacillus spp, Helicobacter pylori.
Chronic catarrhal laryngitis arises as a result of exposure to irritants. The laryngeal epithelium undergoes hyperplasia, with submucosal edema and catarrh observed. The mucosa becomes smooth and hyperemic. The vocal folds are also hyperemic, thickened, and fail to completely close during phonation; mucus is present in the piriform sinuses.
Leading symptoms of chronic catarrhal laryngitis include:
Diagnosis is based on anamnesis and clinical examination. Depending on the clinic’s equipment, indirect laryngoscopy or flexible video laryngoscopy is performed.
The first and most important step in treatment is identifying and removing the causal factor of the inflammation. Smoking cessation and reducing vocal strain are recommended. If the infection extends from the upper or lower airway, it is imperative to manage the primary source.
To control inflammation, inhalations with saline solutions, antibacterial agents, or glucocorticosteroids as needed are advised.
To alleviate inflammation, inhalations with saline solutions, antibiotics, and glucocorticosteroids, if necessary, are advised.
In reflux laryngitis, the etiological factor is cardia insufficiency, causing hydrochloric acid reflux into the upper airway.
Reflux laryngitis is characterized by hyperemia and edema in the interariespace, with mucus accumulation in the piriform sinuses.


Symptoms of Reflux Laryngitis:
Symptoms worsen at night and during sleep.
Diagnosis is based on anamnesis and clinical examination. Indirect laryngoscopy or video laryngoscopy is performed depending on the equipment. In reflux laryngitis, consulting a gastroenterologist, with esophagogastroduodenoscopy and esophageal pH monitoring, is essential.
In reflux laryngitis, prescribed therapy by a gastroenterologist aims to reduce gastric acid secretion. To reduce laryngeal inflammation, saline inhalations, antibiotics, and glucocorticosteroids, if necessary, are indicated.
Atrophic laryngitis is more commonly seen in elderly patients, during hormonal changes (such as menopause), or after long-term exposure to harmful working conditions (high dustiness, harmful chemicals).
In atrophic laryngitis, the number of mucous glands in the larynx diminishes. The mucosa appears parchment-like, thin, dull, and covered with thick, viscous mucus. The vocal folds are also thin and fail to close completely when phonating, leaving an oval glottal gap.
Atrophic laryngitis is characterized by the following symptoms:
Diagnosis is based on anamnesis and clinical examination. Depending on the clinic’s equipment, indirect laryngoscopy or flexible video laryngoscopy is performed.
For atrophic laryngitis, consistent hydration of the mucosa by saline inhalations or oil-based sprays is advised. Mucosal irrigation with iodine solutions incites a mild irritant response, enhancing mucus production.
Fungal laryngitis typically results from chronicization of acute fungal laryngitis. It develops due to poor or incorrect therapy for fungi such as Candida, Aspergillus, Penicillium. More common in immunocompromised patients or those chronically using inhaled corticosteroids.
In cases of fungal laryngitis caused by Candida, white, curd-like deposits are present on the hyperemic mucosa, most commonly on the epiglottis. In aspergillosis, black colonies may be seen on the irritated mucosal surface.
Fungal laryngitis presents with the following symptoms:
Diagnosis is based on medical history and physical examination. Depending on available equipment and protocols, indirect laryngoscopy or flexible video laryngoscopy may be performed. To identify the causative pathogen and assess its antimicrobial susceptibility, a bacteriological examination of laryngeal mucosal samples is performed.
Fungal laryngitis is typically managed with local or systemic antifungal agents.
To hydrate the laryngeal mucosa, saline inhalations are recommended.
This group of conditions encompasses widespread hyperplastic laryngitis and chronic edematous-polypoid laryngitis (Reinke’s edema). Notably, some authors classify Reinke’s edema as a benign laryngeal tumor.
This group of laryngeal disorders occurs predominantly in individuals with voice-dependent professions who misuse or overstrain their vocal cords. It is also commonly observed among smokers and individuals with chronic alcohol use. Less frequently, cases occur in individuals with harmful profession-related factors (dust, paint solvents, textiles, and leather).
Diffuse hyperplastic laryngitis is marked by extensive hyperplasia of the laryngeal mucosa. Various regions of the larynx become symmetrically thickened. Various regions of the larynx become symmetrically thickened. The most commonly affected areas include the free edges of the vocal folds, the arytenoid cartilages, and the interarytenoid region. Hyperplastic growths may lead to significant narrowing of the glottic airway. The mucosa appears hyperemic and uneven.
In edematous–polypoid laryngitis, there is bilateral, gelatinous swelling occurs along the entire free edge of the vocal folds. These folds fail to close completely during phonation, and the glottic airway may become narrowed due to mucosal overgrowth.


The following common symptoms are characteristic of all diseases in this group:
In cases of pronounced mucosal hyperplasia, symptoms may progress to aphonia or laryngeal stenosis secondary to significant airway narrowing.
Diagnosis is based on medical history and physical examination. Depending on available equipment and protocols, indirect laryngoscopy or flexible video laryngoscopy may be performed.
A biopsy combined with microscopic examination — most commonly carried out intraoperatively — is required.
Initial management for all patients includes eliminating contributing factors such as tobacco and alcohol use, excessive vocal strain, and occupational exposure to harmful irritants. Individuals in voice-dependent professions should consult a phoniatrist for targeted vocal therapy.
The treatment approach is typically multimodal and includes both medical therapy and surgical excision of hyperplastic lesions.
Conservative therapy:
Surgical treatment consists of the mechanical removal of altered tissues. Several methods are distinguished:
Postoperative voice rest is essential to support optimal healing and reduce the risk of recurrence.
1. What are the characteristic symptoms of chronic laryngitis?
2. What can be the cause of chronic laryngitis?
3. What complications can arise with chronic laryngitis?
4. What clinical recommendations exist for treating chronic laryngitis?
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