How can Ludwig's angina occur?

Start from dental infections such as pulp necrosis (caused by the left untreated deep caries and periodontal pockets), which provide a way for bacteria to reach the periapical tissue. Due to a large number of bacteria, the infection can spread to the spongy bone to the cortical bone. If the bone is thin, the infection will penetrate and enter the soft tissue. The spread of this infection depends on the resistance of the body's tissues.

The spread of odontogenic infections can be through the connective tissue (percontinuitatum), blood vessels (hematogenous), and lymph vessels. The most common thing is through the connective tissue, because of the gap/space between the tissues that can collect pus.

Infection of the maxilla can form a palatal abscess, submucosal abscess, gingival abscess, cavernous sinus thrombosis, labial abscess, and facial abscess. Transmission of infection to the mandible can form a sublingual abscess, submental abscess, submandibular abscess, Submasseteric abscess, and Ludwig's angina.

The second and third molars' root tips are located behind under the linea mylohyoid (where the mylohyoideus attaches) in the submandibular space, causing an infection in these teeth to form abscesses and pus spreads into the submandibular space, even extending to the pharyngomaxillary space. An abscess in the tooth root that spreads to the submandibular space will cause slight discomfort to the tooth; pain occurs when tension occurs between the bones.

Ludwig's angina, caused by an odontogenic infection, originates from the lower second or third molars. This tooth has roots that lie above the mylohyoid muscle, and an abscess at this location can spread to the submandibular space. Infections that spread beyond the root of the tooth originating from the premolar teeth are generally located in the first sublingual, whereas infections outside the root of the tooth originating from the molars are usually in the submandibular space.

An infection rapidly spreads from the submandibular, sublingual, and submental spaces and causes swelling and elevation of the tongue and muscular induration of the mouth's floor. The potential area for cellulitis inflammation or Ludwig's Angina is the suprahyoid space between the muscles that attach the tongue to the hyoid bone and the mylohyoid muscle. Inflammation of this space causes an excessive force on the oral floor tissue and pushes the tongue up and back and can potentially cause airway obstruction.

The submental space's infection is usually limited because there is a firm union of the deep cervical fascia with m. digastricus anterior and hyoid os. Chin edema can develop clearly.

The infection of the submaxillary space is usually only within the submaxillary space itself. Still, it can also travel along the Wharton submaxillary duct and follow the glandular structure into the sublingual space, or it can extend downward along with the hyoglossus muscle to the fascial areas of the neck.

In sublingual space infections, edema is present in the weakest areas superiorly and posteriorly, pushing the supraglottic larynx and tongue back, eventually narrowing the duct and obstructing the airway.

The spread of infection ends in the anterior part of the mandible and the inferior part, namely m. mylohyoid. The infectious process then proceeds superiorly and posteriorly, extending to the floor of the mouth and tongue. The hyoid bone limits the occurrence of this process inferiorly. Therefore, the swelling extends to the front of the neck. That extended swelling causes a change in the shape and appearance of a "bull neck."



References
1. Leminick M David, MD.  Ludwig’s Angina.  Diagnosis and treatment .Www.turner-white.com.July 2002
2.  Nicholas Costain, BSc, Thomas J. Marrie, MD.  Ludwig’s Angina  DalhousieUniversity, Halifax, Nova Scotia: Canada.2011
3. Aishwarya Balakrishman M.S. Thenmozhi. Ludwig’s Angina: Causes Symptoms and Treatment: journal of pharmaceutical sciences and research. 2014
4. Kavarodi. A.M.  Necrotizing fasciitis in association with Ludwig's angina –  a case report: The Saudi Dental Journal 2011