It is shown in this paper that the infecting organisms in the parodontal sulcus are confined to the surface, but may be forced into the blood and lymph stream by traumatic interference. Local and general disturbances may therefore arise both as a result of the absorption of soluble toxic matter from the pocket into the tissues and also as a result of this traumatic introduction of organisms into the blood-stream. The effect of toxic absorption on the local tissues is destruction of the attachment of the tooth-pyorrhœa. The remote effects of toxic absorption may be a similar destruction of the connective tissue generally-arthritis and fibrositis. The liver and kidney may suffer since they excrete the toxic matter, and other susceptible tissues may also be involved. Traumatic bacteræmia may produce local bone necrosis or “dry” socket. Acute suppurative lymphangitis produces the “pyorrhœtic abscess”. The remote effect of bacteræmia may be to produce osteomyelitis (e.g. of the tibia) or to convert a simple endocarditis into the bacterial type. The mechanism of bone absorption and deposition in response to irritation is discussed. Methods of eliminating parodontal infection are referred to and the importance of complete elimination is stressed. It is shown to be not incompatible with the conservation of the teeth.
Definition.A focus of infection is a chronic lesion where septic organisms have secured a foothold in a necrotic nidus from which soluble toxic matter may diffuse into the adjacent living tissues and be carried thence all over the body. From such a focus these same organisms may sometimes be dislodged by relatively slight traumatic interference and propelled into the bloodstream.The term "focal infection" is applied to that condition of general ill health which arises as a result of the presence in the body over a long period of such a focus. Examples of these foci are the infected root canals of a tooth or the crypt of a tonsil. There is obviously a significant difference between the dissemination of the organisms themselves and the diffusion of their toxic products.Pathology.The organisms concerned in oral infection are principally the streptococci and the group known as viridans is invariably present. The local lesions can, however, all be produced experimentally with any of the septic organisms; and though in the mouth, contaminating organisms enter and complicate the experiment, it is possible to produce quite comparable bone lesions with pure cultures elsewhere in the body, where contamination can be prevented. In this way it can be shown that the local lesions are not specific reactions due to the introduction of one particular organism, but are simply examples of the ordinary reaction of the tissues to septic invasion; and indeed it is equally true that the lesion cannot be produced by merely introducing organisms, whatever they be, into the oral cavity. An animal will lick the pus from a suppurating wound but that will not cause pyorrhoea. The development of a lesion depends entirely on the local terrain and the mode of implantation of the organism. Any of the pus producing organisms will produce the lesion if these are conducive and the infection rapidly becomes a mixed one.The chronicity of the lesion depends on the opportunity offered to the germs to maintain a footing in contact with the tissues, but protected from attack by the polymorphonuclear leucocytes. It is the unique opportunity afforded by the dental tissues for such a footing which makes them a constant source of focal infection.The classical instance is the "dead tooth.
THE case which I have to record is one of compound composite odontome It occurred in a girl of 12 years of age.
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