13: Periodontology

CHAPTER 13 Periodontology

PERIODONTIUM

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.

See Chapters 2, Embryology and Histology: healthy periodontium; 6, General and Oral Pathology: periodontal lesions; 8, Microbiology and Immunology: background information; 11, Clinical Treatment: periodontal evaluation and charting; 17, Community Oral Health: epidemiology of periodontal disease.

Periodontal Diseases and Risk 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 Use Risk

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.

See Chapter 9, Pharmacology: tobacco cessation.

Endocrine Disorder Risk

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.

See Chapters 6, General and Oral Pathology: endocrine diseases; 11, Clinical Treatment: pregnant patient.
D. Alterations in hormones: puberty, pregnancy, oral contraceptives, infertility treatments, perimenopause and menopause ALL affect periodontium (but ALL are temporary because hormonal levels change).

CLINICAL STUDY

Age 25 YRS SCENARIO
Sex image Male image 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.
Height 5′10″
Weight 220 LBS
BP 120/82
Chief Complaint “I gave up smoking and still my gums are a mess. Is it my being pregnant?”
Medical History

Current Medications None Social History Student nurse

Nutritional Deficiency Risk

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.

See Chapter 7, Nutrition: diet counseling.

CLINICAL STUDY

Age 38 YRS SCENARIO
Sex image Male image 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.
Height 6′4″
Weight 185 LBS
BP 105/68
Chief Complaint “My mouth hurts so bad that I can’t eat. And I have not been feeling well lately.”
Medical History

Current Medications OTC ginseng qd Social History Unemployed graphic designer

Neutrophil Abnormality Risk

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.

See Chapters 6, General and Oral Pathology: neutropenias; 8, Microbiology and Immunology: PMN structure and function.

ETIOLOGY OF PERIODONTAL DISEASE

Many factors are involved in the etiology of periodontal disease, including host response, microbiology, oral contributing factors, occlusal trauma.

Defense Mechanisms of Oral Cavity

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.

Inflammatory Response

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.

Clinical Signs of Inflammation

Inflammation is identified by several clinical (cardinal) signs, including gingival bleeding and changes in gingival color, contour, position.

Immune Response

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.

A. Nonspecific host responses (innate host defense mechanisms):

Dental Biofilm

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).

See Chapter 8, Microbiology and Immunology: microbiology overview.
A. Types:

2. Subgingival dental biofilm: located in pockets apical to the crest of marginal gingiva within periodontal pocket.

Table 13-1 Main periodontal pathogens

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

Etiology: Oral Contributing Factors

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.

B. Local predisposing factors: harbor dental biofilm microorganisms, responsible for promoting oral disease.

2. Supragingival and/or subgingival calculus is the MOST significant among this group of factors because it BOTH harbors dental biofilm and consists MAINLY of mineralized dental biofilm.

Jan 1, 2015 | Posted by in Dental Hygiene | Comments Off on 13: Periodontology
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