Medical Conditions Affecting the Periodontal Tissues
When forming a periodontal diagnosis, it is important to be aware of underlying medical conditions that can alter the response of the peiodontal tissues to plaque accumulation, or act independently of plaque on the periodontal tissues.
A thorough medical history is an integral part of the dental examination for new patients, and should be updated at each recall appointment. A number of medical conditions, or their related drug therapy, can lead to gingival hyperplasia. Of the ten or more drugs that have been found to cause gingival overgrowth, the three most common types of drugs that have been associated with hyperplasia are:
- Phenytoin (Dilantin), an anticonvulsant drug used in the management of epilepsy.
- Cyclosporin A (Sandimmun), used to prevent rejection in organ transplantation, and for treatment of some aut~immune diseases.
- Nifedipine (Adalat), a calciumchannel blocker used in the prophylaxis and treatment of angina, and in the control of mild hypertension.
Hormonal effects due to pregnancy, puberty and the contraceptive pill have also been related to gingival hyperplasia. Increased progesterone secretion alters the gingival vasculature and the inflammatory response to accumulated plaque.
Gingival hyperplasia is also associated with some granulomatous disorders, such as Crohn's disease, sarcoidosis and Wegener's granulomatosis. Crohn's disease is the most common of this group. The characteristic gingival lesion associated with this disease is a diffuse erythematous, granular enlargement of the attached gingiva. Severe periodontal destruction has been reported for some patients with Crohn's disease.
It is always necessary to eliminate local causes of gingivalovergrowth. Plaque and ill-fitting dentures are also major causes of this response, and need to be corrected as part of periodontal management. Defects in the host response may lead to more rapid periodontal breakdown. Insuliniiependent diabetes mellitus, particularly if undiagnosed or poorly controlled, is related to increased periodontal destruction and susceptibility to periodontal abscesses. Neutrophil defects related to cyclic neutropenia and leukemia result in severe destructive periodontitis. The periodontal manifestations of genetic conditions, such as Down's syndrome, Papillon-Lefevre syndrome and Chediak-Higashi syndrome, also occur through defects affecting neutrophils. HIV infection dramatically suppresses normal host response, and HIV-related gingivitis and periodontitis have been defined as distinct clinical entities.
There are a few rare connective tissue disorders that result in accelerated periodontal destruction, including scurvy, kwashiorkor (protein deficiency), hypophosphatasia, and Ehlers-Danlos syndrome. Neoplastic disorders, such as squamous cell carcinoma, multiple myeloma, and eosinophilic granuloma, can affect the gingival tissues or the deeper periodontal tissues leading to bone loss. A medical history should not only uncover illnesses that directly affect the periodontal tissues, but should also reveal conditions that may affect your management of the patient. Many common medications result in decreased salivary flow. A history of radiation therapy to the head or neck area can also be related to dry mouth. Disabling conditions such as arthritis can limit the patient's ability to clean their teeth, and oral hygiene devices may need to be adapted to the patient's needs. The need for antibiotic prophylaxis, (for example, due to rheumatic fever, cardiac valvular surgery, prosthetic replacement of hip joints), should be recorded and included as part of a periodontal treatment plan. Allergies to any medication should also be noted.
Smoking has been associated with increased periodontal destruction in some studies, and therefore details of this habit should be recorded. Advice on smoking cessation can form part of your overall treatment plan.
An excellent reference for the relationship between medically related conditions and the periodontium is: Seymour RA, Heasman PA. Drugs, diseases and the periodontium. Oxford University Press, 1992.