Pathways of Periodontal Disease and Alveolar Bone Loss in Type II Diabetes

Abstract

Uncontrolled or poorly-controlled type II diabetes often exhibits a high morbidity of periodontal pathology. Food impaction in defective restorations or open proximal contacts often leads to infection, carious lesions, periodontitis, alveolar bone loss and often tooth loss. An iatrogenic injury occurs when restorations are defective, fractures, or have open proximal contacts and are not planned to be repaired or replaced. In addition to having poor therapeutic outcomes, defective restorations or open contacts may be due to misdiagnosis or errors in treatment planning. Furthermore, drifting of the dentition and ill-fitting crowns, bridge work, or prostheses can result in areas of food impaction. The adverse sequelae of poor therapeutic outcomes are magnified in type II diabetes. The etiology of periodontal disease and alveolar bone loss in type II diabetes consists largely of the following factors: (1) Negative metabolic factors in type II diabetes include unstable glucose homeostasis and regulation, impaired micro/macrocirculation, depressed immune system, defective collagen metabolism, and the presence of a deleterious genetic make-up. (2) Unhealthy behavioral factors impact the severity of type II diabetes including deficiencies in diet, exercise, or oral hygiene and lack of needed dental and medical interventions. These negative sequelae contribute to the proliferation of pathogenic microorganisms in the oral cavity and ultimately dental caries and periodontal disease. Acting both orally and systemically, type II diabetes and its precursor metabolic syndrome are key elements in the development and progression of degenerative changes that constitute periodontal disease and subsequent bone loss. (3) In addition, socioeconomic factors like lack of financial resources, lack of access to dental offices/clinics, lack of transportation, and cultural factors limit receiving ongoing dental care. With the high propensity for diseases of the periodontium in type II diabetes, defective restorations, interproximal caries, and open proximal contacts acting as food traps create a locus for significant pathology. Besides a high incidence of carious lesions, teeth restored without proximal contacts often undergo drift and tipping with associated negative morphological changes in the periodontium, including loss of alveolar bone. As a result of toxins released from the action of bacterial colonies on impacted food, plaque, and calculus, there is subsequently substantial inflammation and infection. Preventing food impaction by maintaining or restoring contacts between the proximal surfaces of adjoining teeth and repairing defective restorations are primary concerns in preventing the morbidity of oral infections. The development of oral infections and their sequelae in type II diabetes produce active loci of disease that ultimately cause loss of alveolar bone and teeth. In the long run, infection, inflammation, and tooth loss negatively impact the overall health of a diabetic patient.