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.

image • See CD-ROM for Chapter Terms and WebLinks.
• 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.

A. Major background risk factors: most NOT able to modify.

1. Age: prevalence increases directly with increasing age as a result of repeated inflammatory episodes during lifetime.
2. Gender: men tend to have higher incidence than women.
3. Race: African Americans have consistently demonstrated higher prevalence than Caucasians.
4. Education: inversely related to increasing levels of education.
5. Income: inversely related to increasing levels of income.
6. Residence: slightly MORE prevalent in rural than in urban areas.
7. Geography: NO significant differences have been noted in the United States.

B. Major systemic risk factors: MOST able to modify somewhat.

1. Tobacco use.
2. Endocrine disorders:

a. Diabetes mellitus.
b. Hyperparathyroidism.
c. Hormonal factors.

3. Nutritional deficiencies.
4. Adverse drug reactions.
5. Stress or psychosocial.
6. HIV/AIDS.
7. Neutrophil (polymorphonucleocyte [PMN]) abnormalities.
8. Genetics: genetic predisposition has been related to inherited systemic diseases and to familial occurrences with some forms (e.g., Down syndrome); NOT able to modify at this time.

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.
A. Tobacco smokers: always double amount the patient reports smoking and one cigar is equal to one pack of cigarettes.

1. Tend to exhibit MORE severe levels of disease: deeper pockets, higher periodontal index scores, greater bone loss, higher rates of attachment loss, more calculus (serves as contributing factor in dental biofilm accumulation, prevents pocket healing) than nonsmokers.
2. Increased prevalence of moderate to severe periodontal disease, directly related to number of cigarettes or cigars smoked per day, number of years, current smoking status.
3. May have altered host response to various forms of periodontal therapy.

a. Carbon monoxide in smoking reduces oxygen concentrations, consequently inhibiting movement of WBCs in gingival sulcus into periodontium (chemokinesis, chemotaxis) and depleting capacity to engulf and destroy bacteria (phagocytosis).
b. Smokers also have decreased levels of salivary antibodies (IgA) and serum IgG and IgM antibodies to P. intermedia and F. nucleatum, two periodontal pathogens.

4. Increased risk for recurrent/refractory periodontitis because of failure to respond to treatment (discussed later).

B. Smokeless (spit) tobacco users:

1. Have LOCAL exposure to high concentrations of tobacco products; may play role in localized attachment loss.
2. At higher risk for various forms of periodontal disease, as well as caries and oral cancer.

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.
A. Diabetes mellitus (DM): genetically associated, debilitating endocrine disorder characterized by glucose intolerance.

1. Types:

a. Type 1: develops before age 30; MUST be controlled with insulin therapy.
b. Type 2: MOST common form occurs after age 40; may be controlled by diet, oral hypoglycemic agents, or LESS frequently, insulin therapy.

2. Associated with high blood glucose levels that result from decreased insulin levels and create variety of systemic effects, including vascular disease, reduced host resistance, increased incidence of periodontal disease.
3. Defective polymorphonucleocytes (PMNs), PMN chemotaxis, microangiopathy of periodontal tissues, increased collagen breakdown, microbial alterations have been cited as rationales for periodontal disease prevalence.
4. Oral manifestations: xerostomia, candidiasis, increased caries, burning mouth, altered taste.
5. Second major risk factor after tobacco use, MAINLY type 1; type 2 with insulin therapy shows a SIMILAR risk.
6. In patients with uncontrolled DM, oral manifestations include multiple periodontal abscesses, velvety red gingival tissues, marginal proliferation of periodontal tissues.

B. Hypothyroidism: associated with occasional gingival hyperplasia.
C. Hyperparathyroidism: excessive production of parathyroid hormone (PT), which helps control calcium metabolism.

1. Caused by benign adenoma or malignancy and results in osteoporosis, multilocular radiolucent jaw lesions, loss of lamina dura, “ground glass” appearance of alveolar bone.
2. Results in MORE rapidly demineralized alveolar bone when occurs in presence of periodontitis.

D. Alterations in hormones: puberty, pregnancy, oral contraceptives, infertility treatments, perimenopause and menopause ALL affect periodontium (but ALL are temporary because hormonal levels change).

1. Puberty: involves increased levels of hormones, which alter capillary permeability and increase fluid accumulation in the gingiva, resulting in increased risk for gingivitis in presence of dental biofilm.
2. Menstruation: even with normal, cyclical hormonal fluctuations has NOT been shown to increase risk of gingivitis; gingivitis has been shown to be actually lower than during ovulation and premenstruation, when hormones may peak.
3. Pregnancy:

a. Strong correlation with development of gingival changes such as gingivitis, gingival enlargement, pyogenic granuloma (pregnancy tumor).
b. Results in increased levels of progesterone, altering capillary permeability and tissue metabolism, making tissues MORE at risk for inflammatory changes in presence of possibly minimal levels of dental biofilm.
c. Associated with high levels of anaerobes, such as Prevotella intermedia (Pi).

4. Oral contraceptives (birth control pills [BCPs]):

a. Drugs that have been shown to elevate hormone levels and thus mimic pregnancy.
b. Therefore affect gingival tissues in manner SIMILAR to pregnancy; place at risk for gingivitis.
c. However, lower doses generally used may NOT affect periodontium.

5. Infertility treatments: women with MORE than three cycles had higher levels of gingival inflammation, bleeding, and gingival crevicular fluid (GFC); severity strongly associated with duration of drugs.
6. Perimenopause and menopause:

a. Related to mucocutaneous disorders such as erosive lichen planus and mucous membrane pemphigoid.
b. Risk for osteopenia and osteoporosis (discussed later).
c. May affect periodontium if on hormone replacement therapy (SIMILAR to pregnancy or BCPs).

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
4 months pregnant
Quit smoking 4 months ago

Current Medications None Social History Student nurse
1. What is the most likely American Academy of Periodontology (AAP) classification of the patient’s condition?
2. What factors are contributing to her condition? Discuss bleeding index used.
3. How should this condition be treated?
4. What information can be given to the patient to help prepare her for other possible complications?

1. Dental plaque (biofilm)-induced gingivitis caused by endocrine system changes. Her pocket depths are no greater than 4 mm and most likely are pseudopockets because signs of inflammation include gingival edema, which causes tissue enlargement.
2. Predominant factor contributing to the patient’s condition is pregnancy. During pregnancy, increased levels of progesterone have been associated with increased risk for gingivitis. Also frequently associated with high levels of anaerobes, such as Prevotella intermedia (Pi). Gingival bleeding index assesses bleeding of the gingival margin in response to gentle probing, used as indicator of gingival health or disease. To score it, divide the total number of areas that bleed by the number of gingival margins examined, then multiply the result by 100 to arrive at a score (percentage).
3. Thorough professional debridement, elevated dental biofilm control measures, and education regarding correlation between the pregnancy and contributing factors will keep the disease under control.
4. Gingivitis associated with pregnancy begins in second or third month and is most severe in second and third trimesters. Moreover, in pregnant women localized enlargements in interdental papillae may form bleeding growths, referred to as pyogenic granulomas (pregnancy tumors). If these lesions occur, most will disappear at end of the pregnancy as hormones become more regulated. The patient should be congratulated for quitting smoking for own health and that of unborn child. Tobacco use is number one factor in periodontal disease; also affects health of child, now during pregnancy and later with presence of second-hand smoke. However, continued gingivitis can still put patient at risk for a preterm low-birth-weight child.

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.
A. Vitamin A deficiency: effect of deficiency NOT known even though involved in synthesis of epithelial cells, proteoglycans, fibronectin, procollagen.
B. Vitamin B2 (riboflavin) deficiency: may affect the oral cavity, causing angular cheilitis, glossitis, oral ulcerations.
C. Vitamin B6 (pyridoxine) deficiency: since involved in carbohydrate metabolism; may induce generalized stomatitis, glossitis, gingivitis, and other oral symptoms.
D. Vitamin B12 (cobalamin) deficiency:

1. May result from diet or may be caused by altered absorption (pernicious anemia).
2. May make gingival tissues MORE at risk for epithelial dysplasia and malignant transformation.
3. Generally accompanied by folic acid deficiency; folic acid is of interest because may reduce gingivitis or phenytoin (Dilantin)-induced gingival hyperplasia.

E. Vitamin C (ascorbic acid) deficiency:

1. Adversely affects periodontal connective tissue, capillary integrity, and wound healing because vitamin C is essential to collagen biosynthesis.
2. When prolonged, may cause scurvy, which induces severe periodontal changes.

F. Vitamin D deficiency:

1. Results in altered levels of plasma calcium and phosphorus, which interferes with mineralization of organic bone matrix; leads to rickets in children and osteomalacia in adults.
2. Results in loss of lamina dura and thinning of cortical plates (radiographically).
3. May cause common dental anomalies, such as delayed development of the permanent dentition, enamel hypoplasia, cemental resorption, open apical foramina, enlarged pulp chambers, and frequent pulp stones.
4. In adults may lead to osteomalacia, which destroys PDL and resorbs alveolar bone; causes replacement fibrous dysplasia.

G. Antioxidants such as beta-carotene; vitamins A, C, E; selenium may be involved in reducing or preventing diseases caused by free oxygen radicals; thus may play role in treating some forms of oral cancer and have been shown to be involved in tissue destruction associated with periodontitis and chronic inflammatory osteoarthritis.
H. Other nutritional disorders:

1. Osteoporosis:

a. Loss of bone mass caused by imbalance of plasma calcium and phosphorus levels; EARLY loss of bone density with osteopenia.
b. Severity of bone loss increases if periodontitis is superimposed on osteoporosis.

2. Protein deficiency (undernutrition): when severe, significantly reduces host defenses and wound healing.

a. In MOST severe forms (kwashiorkor, marasmus, cachexia) exhibits oral changes such as glossitis, angular cheilitis, xerostomia, increased gingival inflammation, periodontal bone loss.
b. Kwashiorkor is also associated with increased incidence and severity of necrotizing periodontal disease, resulting in cancrum oris (noma or oral gangrene).
c. LESS severe forms still affect oral health among alcoholics, anorexics (self-starvation), long-term bedridden and hospital patients, those taking drugs that depress appetite or increase metabolism.

Stress and Psychosocial Risk

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.

Adverse Drug Reaction Risk

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.

• See Chapters 9, Pharmacology: drugs and side effects; 11, Clinical Treatment: management of xerostomia.
A. Gingival hyperplasia (see later discussion for more specifics and for surgical treatment; Figure 13-1):

1. Associated with anticonvulsants (phenytoin), immunosuppressants for organ and bone marrow transplants (cyclosporin); calcium channel blockers (nifedipine, diltiazem, verapamil); cannabis.
2. Decreases effectiveness of dental biofilm removal during oral hygiene care; hyperplasia is increased with poor oral hygiene.
B. Xerostomia (see later discussion of benefits): side effect of many drugs.
image

Figure 13-1 Gingival hyperplasia associated with anticonvulsant drug therapy (phenytoin [Dilantin]).

(From Bath-Balogh M,Fehrenbach MJ: Illustrated dental embryology and anatomy, ed 2, Philadelphia, 2006, Saunders/Elsevier.)

HIV/AIDS Status Risk

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.

• See Chapter 8, Microbiology and Immunology: HIV/AIDS.
A. HIV- associated gingivitis:

1. Linear gingival erythema (LGE): well-defined red band along free gingival margin, with NO bleeding on probing (BoP).
2. Punctate or diffuse erythema of attached gingiva.

B. HIV-associated periodontitis (Figure 13-2):

1. Defined by presence of LGE, attachment loss, cratering in area of interdental col, severe clefting, which often accompanies recession.
2. Treated by conventional nonsurgical periodontal therapy (NSPT) in conjunction with meticulous homecare.
C. AIDS-associated necrotizing ulcerative periodontitis (NUP): see later discussion.
image

Figure 13-2 HIV-associated periodontitis with linear gingival erythema (note gingival Kaposi’s sarcoma [KS]).

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
Tuberculosis 5 years ago
Epstein-Barr infection 2 years ago

Current Medications OTC ginseng qd Social History Unemployed graphic designer
1. What systemic condition is the patient likely to have?
2. What might be causing the severe pain in his mouth?
3. What is the significance of the palatal ulcerations?
4. What treatment for the patient’s oral condition should be discussed?
5. What periodontal maintenance interval is recommended, after his acute problems have subsided?

1. This patient is likely to have HIV/AIDS, based on generalized lymphadenopathy, generalized malaise, linear gingival erythema (LGE; classic sign of HIV), probable candidiasis, oral ulcerations.
2. Severe pain is most likely caused by the open palatal ulcerations. Candidiasis and LGE typically are not painful.
3. Palatal ulcerations are most likely herpetic lesions, since they are on tissue overlying bone; aphthous ulcers are on tissues that do not cover bone.
4. Tactful discussion should include immediate referral to a physician if patient does not reveal his HIV status. His oral condition requires prescriptions for antiviral drug, such as acyclovir, for herpetic lesions and antifungal agent, such as nystatin (Mycostatin), clotrimazole (Mycelex), ketoconazole (Nizoral), for the candidiasis. In addition, povidone-iodine and chlorhexidine rinses (without alcohol because of open sores) would reduce pain and discomfort the patient is experiencing. May need a lidocaine oral rinse to help with eating.
5. All patients with HIV/AIDS should be seen monthly for periodontal maintenance because oral manifestations of the disease, including those of the periodontium, often occur rapidly and are extremely destructive.

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.
A. Neutropenias:

1. Associated with decrease in circulating PMNs.
2. Manifested as skin infections, upper respiratory infections, otitis media, stomatitis, early exfoliation of the teeth, severe gingivitis with ulceration.
3. May be caused by drugs, radiation, Down syndrome, leukemia, DM, tuberculosis, autoimmune disorders.
4. Oral manifestations include gingivitis, aggressive periodontitis, oral ulcerations.
5. When systemic, MOST often are idiopathic.

a. Cyclic neutropenia is a rare condition characterized by neutropenic episodes that persist for 1 week, occur every 3 weeks, and result in sore gingiva, aphthous ulcers, aggressive periodontitis.

B. PMN dysfunctions:

1. Adherence defects: include leukocyte adherence defect (LAD), genetic autosomal recessive defect:

a. Impair successful margination of PMNs, preventing migration to sites of infection.
b. Clinical condition characterized by recurrent bacterial infections, diminished pus formation, prolonged wound healing, leukocytosis.
c. Dental manifestations are characterized by aggressive periodontitis, progressive alveolar bone loss, premature exfoliation of primary and permanent teeth, severe gingival inflammation.

2. Chemotaxis defects: involve impairment of directional migration of PMNs toward attracting molecules such as bacteria.

a. Include several rare diseases and syndromes that involve defects in PMN locomotion and chemotaxis, such as DM, Down syndrome, ulcerative colitis, Job’s syndrome, Chédiak-Higashi syndrome, lazy leukocyte syndrome, Papillon-Lefèvre syndrome (these rare ones discussed later).
b. Associated with aggressive periodontitis.

ETIOLOGY OF PERIODONTAL DISEASE

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

Etiology: Host Response

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.

• See Chapter 8, Microbiology and Immunology, for related discussion.

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.

A. Intact epithelium provides physical barrier between external noxious substances (e.g., bacterial enzymes such as collagenase and other by-products) and deeper lamina propria.
B. Saliva:

1. Functions to mechanically cleanse oral cavity.
2. Buffers acids produced by bacteria from the dental biofilm.
3. Controls bacterial activity.
4. Contains antibacterial components such as lysosomes and lactoperoxidase.
5. Contains secretory IgA for immune resistance against bacteria, food residues, fungi, parasites, viruses.

C. Gingival crevicular fluid (GCF):

1. Increased amount correlated with severity of gingival inflammation.
2. Provides antibacterial action by bringing white blood cells (WBCs, leukocytes) and antibodies into close proximity with bacteria from dental biofilm.
3. Supplies complement factors that serve to initiate BOTH vascular and cellular inflammatory responses that can damage the periodontium.
4. Provides sticky plasma proteins in the sulcus that serve as adhesive for junctional epithelium (JE), keeping it intact.
5. Contains BOTH cellular and organic elements:

a. Cellular elements include bacteria, desquamated epithelial cells, PMNs, lymphocytes, monocytes.
b. Organic components:

(1) C3 and C5a: play role in release of histamine; also facilitate chemotaxis and phagocytosis.
(2) IgG and IgM: function in activation of complement system.
(3) IgG: facilitates phagocytosis.
(4) IgG, IgA, IgM: prevent tissue destruction by neutralizing bacterial endotoxin.
(5) Serum IgA: prevents penetration of antigens across epithelial barriers.

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.

A. Acute phase of inflammation, “FIRST line” of defense; subdivided into vascular response and cellular responses:

1. Vascular response: develops rapidly following initial insult.

a. Provides plasma proteins and fluid necessary for rapid isolation of irritant.
b. Fluid produced is responsible for associated tissue edema.
c. Vascular dilation causes increased blood volume and decreased velocity, resulting in hyperemia.
d. Initial vasoactive response is produced by release of histamine and serotonin by mast cells located in lamina propria.

2. Vascular permeability is sustained by additional chemical mediators:

a. Kinins.
b. Prostaglandins.
c. C3 and C5a from complement system.
d. Lysosomal enzymes released from leukocytes.

B. Cellular response:

1. MAIN defense cell released in acute phase of inflammation is PMN.

a. PMNs leave central stream of blood vessel (margination) and adhere to endothelial walls (pavementing).
b. PMNs escape through endothelial walls by emigration (diapedesis).
c. PMNs move to injured area (migration) by chemotaxis (directed movement).
d. Main function of PMN is phagocytosis (engulfment of foreign objects such as debris and bacteria).

(1) Mature PMNs are capable of living for ONLY few hours in highly acidic environment.
(2) After PMNs die, release enzymatic contents of lysosomes, causing MORE damage.

2. Considerable debris accumulates, requiring addition of defense cells that are capable of living in acid environment.
3. Appearance of macrophages and histiocytes (both are related blood monocytes in connective tissue) signals beginning of next stage of inflammation, chronic phase.

C. Chronic phase of inflammation, “second line” of defense:

1. MAINLY involves chronic inflammatory cells, attracted to area of inflammation by active proteins called lymphokines that are released by lymphocytes to do MORE containment of inflammation.
2. Involves macrophages (within tissue), which function to phagocytose or debride area.
3. Lymphocytes become MAIN cells, in the form of either T cells or B cells.

a. B cells are concerned with humoral immunity; differentiate into plasma cells, which produce specific antibodies (immunoglobulins [Ig]) targeted at immobilizing specific antigens.
b. B cells also produce memory cells that are capable of producing MORE antibodies on demand.
c. T cells are concerned with cellular immunity and are classified as T4 activator cells, T8 suppressor cells, killer (cytolytic) cells.

4. Elevated plasma C-reactive protein (CRP) is noted with periodontal disease; may be future predictor (inflammatory marker) for activity of disease (similar to cardiovascular disease); periodontal therapy would then seek to modify levels of CRP. However, it is NOT considered specific enough for use during diagnostic procedures.

D. Repair phase of inflammation:

1. Begins when macrophages debride site.
2. Involves fibroblasts from surrounding connective tissue that migrate to injured area and begin to secrete tropocollagen (precursor to collagen) to produce fibrotic (scar) tissue.
3. Involves endothelial cells that proliferate and provide MORE oxygen tension.
4. Involves development of granulation tissue, composed of fibroblasts, new immature collagen, new capillaries.

Clinical Signs of Inflammation

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

A. Gingival bleeding on probing (BoP):

1. Characteristic of the tissue destruction that occurs during acute inflammation.
2. Results from vascular engorgement, increased blood flow, loss of vascular wall integrity, and microulceration of the sulcular epithelium (SE) initially and then later also JE, which exposes deeper lamina propria.
3. May be spontaneous or may follow provocation.
4. MOST reliable sign of acute inflammation, although late sign; lack indicates gingival health.

B. Gingival color changes:

1. Occur during BOTH destructive and proliferative stages of inflammation.
2. Result from thinning of epithelial layers, decrease in keratinization, engorgement of subepithelial blood vessels, capillary proliferation.
3. Bright red color occurs during acute stage of inflammation and is associated with vascular hyperemia.
4. Bluish color is associated with chronic inflammation and venous stasis.

C. Changes in gingival consistency:

1. Occur during either destructive or proliferative stage of inflammation.
2. Include edema, softness, friability during acute inflammation.
3. Caused MAINLY by accumulation of tissue fluid during acute stage of inflammation, thinning of the epithelial layers, loss of keratin.
4. Result in increases in density of tissues during chronic and repair stages of inflammation; these occur because of proliferation of fibroblasts, which produce collagen in the form of scar tissue, giving firm, fibrotic consistency.

D. Changes in surface texture:

1. May include loss of stippling if stippling was present during gingival health.
2. Loss of stippling appears as shiny surface; caused by loss of keratin, thinning of epithelium, accumulation of connective tissue fluid.
3. Loss of stippling is LEAST reliable sign of inflammation.
4. Also changes in gingival contour occur as result of either increased tissue fluid (edema) or increased cellular elements (fibrosis); result in rolled margins and blunted interdental papillae.

E. Changes in gingival position:

1. ALL relative to CEJ; result in increased height of gingival margin because of edema and tissue proliferation.
2. Result in recessed margins, which have numerous causes ranging from edema, to toothbrush abrasion, to malposed teeth.

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):

1. Inflammatory response:

a. Arachidonic acid cascade: produces several biologically active products, including prostaglandins, leukotrienes, thromboxane.
b. MOST notable effects are vascular permeability and attraction of phagocytic cells.
c. Also attract antibodies and complement that aid in destruction of bacteria and their by-products.
d. Products of arachidonic acid cascade are potentially harmful to periodontal tissues and are part of the pathogenesis of periodontal disease.

2. Complement system:

a. More than 20 serum proteins become activated during inflammation and exhibit potent biological activity.
b. Activated through classical pathway or alternate pathway.
c. Effects of activation (by either pathway):

(1) Production of opsonins that enhance phagocytosis (see below).
(2) Mast cell release of histamine that causes vasodilation.
(3) Release of chemotactic factors that causes migration from the blood system of PMNs and macrophages to specific sites.
(4) Production of factors capable of destroying bacterial cell walls.

3. Phagocytic system:

a. Consists primarily of PMNs and macrophages.
b. Phagocytes kill bacteria in two different ways:

(1) Oxygen-dependent system: bacteria are destroyed in phagolysosome in the cell itself, by lysosomal enzyme called myeloperoxidase.
(2) Non-oxygen-dependent system: enzymes and other cationic proteins (e.g., neutral proteases, acid hydrolases) in lysosomes of PMNs and macrophages degrade bacteria after they have been ingested.

B. Specific host responses mediated by lymphocytes:

1. T cells provide cellular immune response:

a. Release of cytokines that include potent products, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta, that are capable of inducing bone resorption.

2. B cells provide humoral immune responses by producing plasma cells that in turn produce specific antibodies and immunoglobulins (Igs):

a. Prevent bacterial cell walls from attaching to oral surfaces.
b. Trigger activation of complement system.
c. Neutralize toxins and enzymes released by bacteria.

3. In addition, white blood cells (WBCs) produced by immune response to bacteria release a family of enzymes called matrix metalloproteinases (MMPs), which break down connective tissue, such as that within the periodontium.

Etiology: Microbiology

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 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:

1. Supragingival dental biofilm:

a. Found coronal to the margins on clinical crowns of teeth or within sulcus or pseudopocket:

(1) With healthy gingiva:

(a) Composed MOSTLY of cocci and rods that are gram positive and aerobic.
(b) Equal percentages of gram-positive cocci and Actinomyces; LESS than 15% are anaerobic.

(2) With early gingivitis: increased numbers of anaerobic, gram-negative cocci and rods.
(3) With chronic gingivitis: increased numbers of anaerobic, gram-negative, filamentous organisms, fusobacteria, spirochetes.
(4) Microbial microcosm increases in complexity by means of progressive, sequential colonization on clean tooth:

(a) Formation of acquired pellicle from salivary proteins on tooth surface.
(b) Attachment by microorganisms (via specific mechanisms), which colonize over time: first, gram-positive aerobic cocci, then gram-negative anaerobic rods, then motile organisms (i.e., spirochetes).

b. Within pits and fissures: morphology allows growth; MOSTLY Streptococcus mutans, Actinomyces naeslundii.

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

a. Diseased periodontium: MORE anaerobic because subgingival area provides LESS oxygen tension, which is MORE conducive to anaerobic growth.
b. During active periodontal disease: MOSTLY anaerobes at >90% of organisms present, typically with 75% of them gram-negative organisms; there are also large numbers of gram-negative, facultative anaerobic organisms.
c. Divided into three zones (LOCATION LOCATION LOCATION—hey, real estate is real estate):

(1) Tooth-attached: attached along tooth surface from gingival margin almost to the JE at base of pocket.

(a) MOSTLY gram positive, although gram-negative cocci and rods present.
(b) Associated with calculus formation, root caries, root resorption.

(2) Epithelium-attached: loosely attached to inner lining.

(a) Layers closest to pocket lining have large numbers of motile, gram-negative, anaerobic microorganisms and spirochetes.
(b) Microorganisms are seen invading ulcerated inner pocket lining into lamina propria and have been found on outer portions of alveolar bone; MAINLY involves Aggregatibacter (previously Actinobacillus) actinomycetemcomitans (Aa) and Treponema denticola (Td).
(c) Relative proportions are related to nature of disease activity; MOSTLY associated with gingivitis and periodontal disease.
(d) MOST virulent and detrimental portion of dental biofilm to periodontium.

(3) Unattached: free-floating in pocket; since pocket has LESS mechanical stress, attachment is NOT vital; at base of pocket is MAINLY unorganized gram-negative rods and spirochetes, separated from inner pocket lining by WBCs.

d. The pH is regulated MAINLY by saliva; from 6.75 to 7.25 (see more information in Chapter 11, Clinical Treatment).
e. There is a consistent distance from dental biofilm to alveolar bone that is never <0.05 mm and never >2.7 mm; microorganisms can cause destruction of alveolar bone crest only when it is <3 mm away from dental biofilm.

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

Bacteria-Mediated Tissue Destruction

Tissue destruction mediated by bacteria is caused by release of toxins and enzymes from these microorganisms.

A. Bacterial enzymes (hyaluronidase, collagenase, ribonuclease) affect host cells and intercellular (ground) substance; proteolytic and hydrolytic enzymes destroy cells and increase permeability of epithelial and connective tissues.
B. Bacterial cell walls of microorganisms that are released at the time of their destruction:

1. Gram-negative: lipopolysaccharides (LPS, endotoxin):

a. Activate alternate pathway of immune complex fixation process (via complement).
b. Side reaction proteins are BOTH chemotactic and cytolytic (C3, C5, C5a).

2. Gram-positive: lymphotoxins (LT, exotoxin):

a. Inhibit the chemotactic response of the host cells.
b. Inhibit host cell phagocytosis.
c. Create resistance to killing and digestion within phagolysosomes of host cells.
d. Release toxins that are cytolytic and/or cytotoxic.

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.

A. Local functional factors: weaken the PDL, widening the PDL space and thus promoting dental biofilm accumulation; include missing teeth, malocclusions, tongue thrusting and mouth breathing habits, parafunctional habits such as chewing on pencils or other foreign objects, traumatic occlusion (discussed next).
B. Local predisposing factors: harbor dental biofilm microorganisms, responsible for promoting oral disease.

1. Include calculus, materia alba, dental stains, faulty restorations and overhangs, food impaction, untreated caries, tooth anatomy (e.g., furcas).
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.

a. Supragingival calculus: mineralized supragingival dental biofilm from salivary minerals.

(1) Found coronal to margins on clinical crowns of teeth, typically yellowish white; may darken with age or dietary staining.
(2) Found MOST commonly on lingual surfaces of mandibular anteriors and on buccal surfaces of maxillary first and second molars; BOTH adjacent to salivary gland ducts that promote mineralization of dental biofilm.
(3) Found LEAST on occlusal surfaces because of mastication.
(4) Composed of MAINLY inorganic (70% to 90%) and some organic (10% to 30%) content.

(a) Inorganic mineral component is made up MAINLY of calcium phosphate (75.9%) and calcium carbonate (3.1%), with traces of magnesium, sodium, potassium, fluoride, zinc, strontium.
(b) Organic component is mixture of protein-polysaccharide complexes, desquamated epithelial cells, leukocytes, carbohydrates, lipids, glycosaminoglycans, various types of microorganisms.

(5) Primary crystalline structure is MAINLY calcium hydroxyapatite, Ca10(PO4)6(OH)2; includes smaller amounts of octocalcium phosphate, whitlockite, brushite.

b. Subgingival calculus: mineralized subgingival dental biofilm from GCF’s minerals, which are originally from associated gingival tissue blood supply.

(1) Located in sulcus and pockets apical to the crest of marginal gingiva; typically is dense, hard, dark brown or black, firmly attached to root surface.
(2) Composition differs slightly from that of supragingival calculus, MAINLY by higher ratio of calcium to phosphate and increased sodium.
(3) Normal mode of attachment to the tooth is by means of salivary acquired pellicle; mineralization occurs within 24 to 72 hours, and maturation occurs in an average of 12 days.
(4) May form MORE tenacious attachment by penetrating cementum and/or mechanically locking into surface irregularities, making removal difficult (YES!).

c. Rate of calculus formation varies among individuals, may also vary among teeth; calculus may be light, moderate, or heavy.

3. Food impaction: forceful wedging of food into periodontium by occlusal forces, which leads to dental biofilm retention.
4. Food debris:

a. Although rapidly cleared away from oral cavity, tends remains on the teeth and oral mucosa.
b. Cleared from mouth by salivary flow and mechanical action of tongue, cheeks, and teeth.
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Related posts:

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  2. 7: Nutrition
  3. 8: Microbiology and Immunology
  4. 14: Pain Management
  5. 6: General and Oral Pathology
  6. 3: Anatomy, Biochemistry, and Physiology

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

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