CHAPTER 13 Periodontology
Periodontium consists of gingival tissues, periodontal ligament (PDL), cementum, alveolar bone. Functions as attachment mechanism, shock absorber, line of defense against external agents; attaches the tooth to its bony housing (alveolus), provides resistance to forces of mastication, speech, and deglutition, maintains body surface integrity by separating the external and internal environment, adjusts for structural changes associated with wear and aging through continuous remodeling and regeneration, and defends against external harmful factors.
Periodontal (gum) diseases, including gingivitis and periodontitis, are serious infections that, left untreated, can lead to tooth loss. Periodontal pathogens alone may NOT lead to development of disease. Degree of destruction varies greatly from one individual to another, which suggests that other factors may alter host’s resistance. These factors have been labeled risk factors.
Risk factors affect prevalence, incidence, severity, development of a disease—periodontal disease in this case. Some of these factors, such as genetics and age, are beyond individual’s control but others, such as tobacco use or stress factors, can be modified. Even endocrine disorders, nutritional deficiencies, drug reactions, HIV status can somewhat be modified. Increased incidence of periodontal disease may in turn represent a risk factor for cardiovascular disease (CVD) or birth of preterm, low-birth-weight baby, as well as pose a serious threat to people whose health is compromised by diabetes mellitus, respiratory diseases, or osteoporosis.
Tobacco is the MOST important risk factor involved in periodontal disease. Nicotine and other chemicals embed on the root surface and act as toxic irritants, in addition to causing constriction of area blood vessels. Result is that tobacco users are at greater risk for periodontal disease and LEAST likely to heal after treatment. Thus it is the MOST traumatic habit for periodontium and the hardest to modify, but when tobacco ceases to be a risk factor, it is the MOST effective part of the overall therapy for periodontal disease.
Endocrine glands secrete hormones that regulate cellular metabolism and maintain physiological homeostasis. Endocrine diseases, such as diabetes mellitus and hyperparathyroidism, have been associated with greater risk of periodontitis; MOST can be modified with treatment. Fluctuations in hormones (through puberty, menstruation, pregnancy, oral contraceptives, perimenopause or menopause) have also been shown to alter tissue response to local factors and therefore are risk factors for development of gingivitis and periodontitis, although MOST changes are temporary.
|Sex||Male Female||The patient, whom the dental office has been seeing regularly every 6 months for oral prophylaxis, presents with pocket depths that have increased from 3 to 4 mm and a bleeding score of 60%, according to the Ainamo and Bay bleeding index. Signs of gingival inflammation are present in the form of marginal erythema, generalized bulbous interdental papillae, and rolled margins. This finding is unusual for the patient because she has always exhibited meticulous oral hygiene. Moreover, dental biofilm and calculus are not present in noticeable quantities during this visit.|
|Chief Complaint||“I gave up smoking and still my gums are a mess. Is it my being pregnant?”|
Poor nutrition lowers resistance to periodontal disease, which makes deficient individuals MORE at risk for infection and severe forms of periodontitis. In United States, nutritional deficiencies are found MOST commonly among elderly, lower socioeconomic groups, drug and alcohol abusers. Food consistency also has been recognized as contributing factor to accumulation of dental biofilm and thus development of periodontal disease. Poor nutrition can be modified with proper diet.
Increased risk for and severity of periodontal disease have been reported during stressful life events such as death, divorce, war. Plasma corticosteroid levels become higher during exposure to stressful stimuli and act to suppress protective portions of immune response. Strongest example of correlation between stress and periodontal disease is necrotizing periodontal disease (discussed later). Stress can be minimized and controlled and in MOST cases is temporary in nature.
Drugs may have a variety of adverse effects in the oral cavity, ranging from allergic to toxic reactions, including gingival hyperplasia and xerostomia. Although drugs themselves do NOT cause periodontal disease, may provide locally irritating conditions that place individual at risk. Unless a drug is taken indefinitely, MOST side effects would be temporary and able to be modified by time.
Oral manifestations of HIV infection often are first signs of AIDS. Dental hygienist may be the first person to identify such manifestations because of seeing patients often over time. Prevalence of periodontal disease and other oral manifestations in patients with HIV/AIDS varies significantly, depending on decline of immune system, lifestyle, early recognition, treatment, ALL of which can modify it as a risk factor.
|Sex||Male Female||Patient has a chronic cough that he notes has persisted for several months. The extraoral examination reveals bilateral generalized lymphadenopathy. Intraorally, several large ulcerations that are red and raw are noted on the hard palate. Additionally, a thick white coating appears on portions of the hard palate and all of the soft palate, extending into the pharynx; when the coating is wiped off with gauze, raw inflamed tissue is exposed. The gingival tissues have a definite red band along the facial gingival margins of the maxillary arch; however, no bleeding is detected.|
|Chief Complaint||“My mouth hurts so bad that I can’t eat. And I have not been feeling well lately.”|
The MAIN etiological factor in development of gingivitis and periodontitis is dental biofilm. Also recognized that bacteria and host response MUST be in balance to avoid disease. One of the MAIN players in active host response is the PMN. When PMN response is impaired, bacteria flourish and disease often becomes MORE severe. Most cases of altered host response are NOT able to be modified at this time as risk factors, unless resulting from treatment and drug use.
Bacteria interact with host in MOST cases of periodontal disease. In healthy individuals, active host response quickly results in slight inflammation, which destroys the antigens (bacteria). However, periodontal health depends on balance between BOTH protective and destructive systems. When host response is impaired, MORE rapid destruction of periodontium results. Included in host response are the defense mechanisms of the oral cavity, inflammatory response, immune response, all discussed next. See also later discussion of pathogenesis of periodontal disease for host response to etiological factors over time.
Natural defense mechanisms that exist in the oral cavity include intact epithelium, saliva, gingival crevicular fluid. Mechanisms work together to defend against mechanical, bacterial, chemical aggression.
Inflammation is the natural response to insult; divided into three phases that include acute, chronic, repair. NOT only does inflammation seek to fight the insult, it also adds insult to injury against the periodontium.
Immune response is a complex entity that consists of BOTH nonspecific and specific components. Because of large numbers of bacteria that inhabit the oral cavity, effective host response is required to minimize disease and tissue destruction. Important to recognize that majority of tissue damage produced during periodontal inflammation is caused by the host’s response to bacteria. Evidence now suggests that periodontal disease is possibly an autoimmune disorder, in which immune factors in the body attack the person’s own cells and tissue—in this case, those in the gingival tissues.
Strong relationship exists between microbial dental biofilm and periodontal disease. However, constant presence of microorganisms in the oral cavity and its relationship to disease is a complex issue that involves MANY factors, including host response, microbial virulence, genetics. Periodontal disease is essentially a disease caused by bacteria. However, mere presence of bacteria does NOT preordain disease. Host defense mechanism of the individual is the balancing factor in maintenance of health. If BOTH bacterial load and host response are in balance, NO disease occurs. If either a critical mass of bacteria is reached or host response is somehow impaired, disease occurs. Etiology therefore should be discussed from perspective of BOTH host response and bacteria.
Dental biofilm (dental plaque) is a living, highly organized, and complex microbial ecosystem composed of more than 300 species of bacteria embedded in a gelatinous matrix. Classified as either supragingival or subgingival. Microflora associated with each type of periodontal disease classification as noted in the Human Oral Microbiome Database (HOMD) are listed in each subcategory, as well as Table 13-1. Presence of dental biofilm (and associated calculus) is the MOST common reason for gingivitis (NOT more obscure causes such as vitamin C deficiency).
|Microorganism||Gram stain reaction, motility||Associations|
|Aggregibacter (previously Actinobacillus) actinomycetemcomitans (Aa)||Gram negative, nonmotile||Chronic periodontitis (less than with Pg) and aggressive periodontitis, both localized and generalized; can invade tissue|
|Tannerella forsythensis (Tf) (previously Bacteroides forsythus [Bf])||Gram negative, nonmotile||Early stages of gingivitis and chronic periodontitis|
|Campylobacter rectus (Cr)||Gram negative, motile||Chronic periodontitis|
|Porphyromonas gingivalis (Pg)||Gram negative, nonmotile||Chronic periodontitis (most prevalent) and generalized aggressive periodontitis|
|Prevotella intermedia (Pi)||Gram negative, nonmotile||Gingivitis with pregnancy and chronic periodontitis|
|Treponema denticola (Td)||NA, motile||Chronic periodontitis; can invade tissue|
Although dental biofilm has been recognized as MAIN etiological factor in initiation and progression of gingivitis and periodontitis, other oral contributing factors play a role in retention of dental biofilm. These factors may be divided into local functional factors and local predisposing factors.