Ludwig's angina: An anatomic study of the role of the lower molar teeth in its pathogenesis

Abstract

A brief review of the history of Ludwig's angina is given. According to Ludwig's description, this entity is characterized by gangrenous cellulitis originating in the submandibular (submaxillary) space and rapidly spreading toward the floor of the mouth. Neither isolated cellulitis in one of these spaces nor suppurative submaxillary lymphadenitis can be regarded as Ludwig's angina. For the second condition which sometimes appears as a comparatively benign imitation of Ludwig's angina, the term “pseudo angina Ludovici” or “pseudo Ludwig's angina” is suggested. The frequency of the dental origin and the almost exclusive involvement of the molar teeth in Ludwig's angina are emphasized on the basis of data compiled from the literature. The incompetency of the explanations usually given for the predominant role of the molar teeth in the genesis of Ludwig's angina is shown particularly on account of anatomic studies. In an attempt to find a solution of the problem of the genesis of this disease, anatomic examinations were undertaken to determine the relation of the roots of the molar teeth to the mylohyoid ridge. These showed that the second and third molar teeth almost invariably reach as for as, or even below, the mylohyoid ridge, that the first molar tooth in most instances reaches a point above the ridge, and that the tips of the roots of the anterior teeth are exclusively above this ridge. These findings explain the fact that an infection arising from an infected molar tooth, especially a second or a third one, usually extends into the space below the mylohyoid muscle. Statistics concerning the involvement of the three molar teeth in the etiology of Ludwig's angina were compiled from the literature. They show a striking similarity to these anatomic findings. Attention is called to the report of an autopsy in a case of Ludwig's angina, which showed a perforation of the inner plate of the mandible below the mylohyoid ridge which resulted from a carious process in a second lower molar tooth. In another case, in which the infection started from a premolar tooth, the perforation was located above the attachment of the mylohyoid muscle. The result here was sublingual cellulitis. These reports are recalled because they represent clinical support for the anatomic findings mentioned. I particularly wish to thank Dr. Samuel Iglauer for his aid. It is a pleasant duty for me to acknowledge his interest in the problem, his many helpful suggestions and objective criticisms. I also wish to express my gratitude to Dr. Samuel Brown and Dr. Archi Fine for making the x-ray pictures.