Gingivitis & Periodontitis

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A local irritant and an inflammatory response are both necessary to cause changes to the periodontal tissues. The initiator of periodontitis is most often bacteria within subgingival and supragingival plaque and calculus. This microbial challenge results in an inflammatory response within the periodontal tissues, leading to increased:

inflammatory cytokines.
prostanoids.
enzymes.
antibodies.
polymorphonuclear leukocyte infiltration.

The upregulation of pro-inflammatory mediators are responsible for the connective tissue changes that lead to the clinical signs and symptoms of periodontal disease. The severity of the periodontitis is influenced by:

environmental risk factors such as tobacco use.
acquired risk factors such as systemic diseases (Diabetes).
genetic susceptibility.

INFLAMMATION

Inflammation is a generic immune response considered part of a person’s innate immunity. Innate (non-specific) immunity involves first-line defensive barriers such as skin and mucous membranes, certain behaviors (cough reflex), certain proteins/enzymes (tears, skin oils), and stomach acid. Acute inflammation is initiated by cells normally present in all tissues, including macrophages, dendritic cells, histiocytes, Kupffer cells, and mast cells. These are either permanently present or are quick to respond to a foreign entity, compared to the adaptive immune responses which may take a week or more to become effective. Inflammation is designed to eliminate the initial cause of tissue injury and necrotic tissue, and to promote healing and tissue repair. The five cardinal signs of inflammation are:

Redness (Rubor) – caused by increased blood flow.
Heat (Calor) – caused by increased blood flow.
Swelling (Tumor) – caused by increased cellular permeability.
Pain (Dolor) – damage to cells lead to the production and release of bradykinin and prostaglandins.

Gingivitis leads to visible changes to the soft tissue

color changes are due to increases in blood flow.
contour changes are due to edema.
consistency changes are also due to fibrosis.

PHASES OF INFLAMMATION

There are two phases of acute inflammation. The first is the vascular phase. Initially after tissue injury there is a sudden, temporary constriction of blood vessels caused by the contraction of the smooth muscles in the blood vessel walls (vasoconstriction). This can be seen as blanching around the site of injury. Vasoconstriction is followed by blood vessel widening (vasodilation) to increase blood flow to the area. An increase in vascular permeability allows diffusible components of the blood and specialized cells to enter the site of injury. Tissue injury or the presence of foreign material activates complement and other cellular mediators.

The cellular phase starts with the infiltration of white blood cells (leukocytes). Vascular dilation and increased vascular permeability slows blood flow and allows the circulating leukocytes to aggregate on the inner surface of the blood vessels (margination). These white blood cells, primarily polymorphonucleocytes (PMNs), begin to “squeeze” between the contracted endothelial cells (diapedesis) and migrate to the site of injury (chemotaxis) along a chemical gradient of powerful chemotaxins such as C5a, IL-8, LtB4, and the bacterial protein N-fMLP. PMNs function to engulf (phagocytose) foreign or dead matter, which creates a lipid vesicle around the material (phagosome) inside the cell. Lysosomal granules containing a powerful mixture of oxygen radicals (H2O2, O2−) and granule enzymes (myeloperoxidase) fuse with the phagosome forming a phagolysosome, facilitating material breakdown.

CELLULAR STAGES OF INFLAMMATION

Macrophages are present in all tissues but are more numerous during the cellular stage of inflammation. They have a similar function to PMNs, responsible for the phagocytosis of foreign material, but live much longer in the tissues than neutrophils. Macrophages are also important for immune response regulation by “presenting” ingested antigens to the cells of the specific immune response, and through the release of chemical signals called cytokines. There is a strong reciprocal interaction between macrophages and lymphocytes. When T cells are activated they release macrophage-activating cellular mediators, and when macrophages are engaged they release lymphocyte-activating cytokines. Macrophages may be identified based on their location:

Histiocytes – aka tissue macrophages or dendritic cells, found throughout the body.
Kupffer cells – aka stellate macrophages, specialized cells localized in the liver.
Dust cells – aka alveolar macrophages or pulmonary macrophages, found in the airways.
Microglia – neuroglia found throughout the brain and spinal cord.

The cellular shift within the periodontal tissues from PMNs to macrophages represents the transition to chronic stage inflammation. Gingivitis does not involve loss of attachment or bone. After the cessation of oral hygiene the following stages are expected:

Transient stage/initial lesion (2-4 days) – marked by vascular dilation and vasculitis, with detectable dilation of vessels close to the junctional epithelium. Bacteria and shed epithelial cells can be detected in the gingival sulcus. Clinically there is an increase in gingival fluid flow. Polymorphonuclear neutrophils (leukocytes) are the predominant immune cells present.
Early lesion (4-7 days) – polymorphonucleocytes appear in the gingival sulcus and connective tissues. Vascular proliferation may be evident. The most common leukocytes are lymphocytes, macrophages, plasma cells (produce IgG), and mast cells (produce histamine). Clinically gingival edema is visible. Lymphocytes are the predominant immune cells present.
Chronic stage/Established lesion – inflammatory exudate combined with changes in lamina propria and an increase in plasma cells and B-lymphocytes. Collagen destruction and gingival crevicular fluid that contains fibrin, immunoglobulins, macrophages, lymphocytes (B and T cells), and complement. It is possible for this stage of disease to persist for years without progressing to the advanced lesion or periodontitis. Plasma cells are the predominant immune cells present.

White blood cells (leukocytes) are produced and derived from multipotent cells in the bone marrow known as hematopoietic stem cells. The different leukocytes can be classified by cell lineage. Myeloid cells (myelocytes) include neutrophils, eosinophils, mast cells, basophils, and monocytes (dendritic cells and macrophages). Lymphoid cells (lymphocytes) include helper T cells, memory T cells, cytotoxic T cells, B cells, and natural killer cells. Granulocytes include neutrophils, eosinophils, and basophils. Cells most associated with acute inflammation include basophils, tissue mast cells and platelets. Elevated levels of eosinophils are often indicative of parasitic infections. Elevated levels of lymphocytes (instead of neutrophils) are often indicative of viral infections. Lymphocytes are considered part of the specific immune response, responsible for targeted antigen-specific reactions to foreign material.

Many types of cells are part of the inflammatory process, but leukocytes are important for controlling all three stages (immediate, acute and chronic). These cells originate in the bone marrow and are attracted to zones of inflammation, where they penetrate the endothelial layer (transendothelial migration) and diffuse through inflamed tissue. The primary group of cells that initially migrate to a site of injury are neutrophils, but with time macrophages become more numerous. Neutrophils, monocytes (macrophages), mast cells, and dendritic cells are considered to be part of the innate immune response.

Mast cells are mobile cells that originate in bone marrow and are found in all connective tissues. A relatively high concentration of mast cells can be found in human gingival tissues, and their numbers increase proportional to the extent of inflammation in these tissues. They contain cytoplasmic granules (lysosomes) that release heparin and histamine in response to tissue injury, and are important in immediate inflammatory responses (allergic reactions). Antigen-antibody complexes that become bound to mast cells can initiate the extensive degranulation responsible for an anaphylactic response. Histamine release causes vasodilation and increased vascular permeability by inducing smooth muscle relaxation (vascular phase of acute inflammation). Histamine can also be found in platelets and basophils. Mast cells are able to phagocytose, process and present antigens to cells such as T cells. They have receptors for the complement components C3a and C5a, as well as receptors for the Fc portion of IgE and IgG antibodies. Mast cells may be activated by non-immune processes like stress.

B-cells are white blood cells that differentiate into antibody-producing plasma cells and are important in antibody-mediated immunity. This activation process occurs when the cell is exposed to a specific antigen. Activated B-cells are often found in the spleen and lymph nodes where they produce plasma cells and memory cells. The immunoglobulin IgG is produced by plasma cells and is most characteristic of gingivitis. IgA may also be detected, found mostly in saliva. IgM is not characteristic of gingivitis. Lymphocytes are mostly strongly associated with earlier stages of gingivitis. Plasma cells are most strongly associated with chronic stage gingivitis.

T-cells are white blood cells that mature in the thymus and are important in cell-mediated immunity, type IV hypersensitivity reactions, and amplification and modulation of antibody-mediated immunity. Examples include helper T-cells (CD4 receptor), suppressor T-cells, and cytotoxic T-cells (CD8 receptor). T cells are known to release pro-inflammatory, macrophage-activating chemical mediators. Natural killer cells (NK cells or large granular lymphocytes (LGL)) are a type of cytotoxic lymphocyte that recognizes and kills certain tumors and virally infected cells.

Dendritic cells are leukocytes with dendrites, cellular appendages that facilitate communication between cells. They are antigen presenting cells distributed throughout the tissues and are important in the specific immune response. Langerhans cells are an example of dendritic cells that are often found adjacent to squamous epithelium.

CLASSIFICATION OF HYPERSENSITIVITY

Recall the Coombs and Gell classification of hypersensitivity:

Type I: reaction mediated by IgE antibodies bound to mast cells. When an allergen binds to these antibodies it causes IgE cross-linking and degranulation of mast cells. Examples include localized and systemic anaphylaxis, seasonal allergies (hay fever), and food allergies.

Type II: cytotoxic reaction mediated by IgG or IgM antibodies. Cells are destroyed when the antibodies bind to them, either by the activation of complement or the activation of cytotoxic T cells with an Fc receptor that matches the antibody’s structure. For example, the destruction of red blood cells during a mismatched blood transfusion.

Type III: reaction mediated by immune complexes. Antigen-antibody complexes cause the activation of complement which attracts neutrophils. Examples include glomerulonephritis, rheumatoid arthritis and systemic lupus erythematosus.

Type IV: delayed reaction mediated by cellular (T-cell) response. The antigen engulfed by the macrophages and monocytes is presented to T cells, which then becomes sensitized and activated, releasing cytokines and chemokines. Other cells, such as monocytes, eosinophils, and neutrophils can be involved. Type IV reactions usually occur more than 12 hours after exposure to the allergen, with a maximal reaction time between 48 and 72 hours. Examples include contact dermatitis and drug hypersensitivity.

GINGIVAL CONDITIONS

Drug-induced gingival hyperplasia is a hyper-reactive tissue response caused by certain medications. It can lead to swelling, bleeding, and unaesthetic gingival enlargements. The medications are thought to exacerbate the gingival response, but an initiating factor is still required (plaque). Proper oral hygiene may prevent drug-induced hyperplasia. Gingival hyperplasia can be caused/exacerbated by many medications, including:

Anticonvulsants – Phenytoin (Dilantin).
Immunosuppressants – Cyclosporine A, Mycophenolate.
Calcium channel blockers – Nifedipine, Verapamil, Diltiazem, Felodipine, Amlodipine.
Antidepressants – Sertraline.
Antipsychotics – Pimozide.
Antiviral/antineoplastic – interferon alpha-2-beta.

Pregnancy gingivitis is a hyper-reactive tissue response caused by increased levels of circulating estrogen, progesterone, and other metabolites. Elevated gonadotropic hormones like estradiol and progesterone may lead to increased levels of Prevotella intermedia and Capnocytophaga species in the bacterial plaque, likely because these hormones act as a menadione (growth factor) substitute. Hormonal changes cause increased gingival vasculature and tissue permeability. When present, pregnancy gingivitis often increases in severity in the second or third month of pregnancy, and chronic irritation or trauma may cause a localized benign overgrowth termed a pregnancy epulis or pregnancy tumor (not a true neoplasm). Pregnancy gingivitis is usually self limiting during the final trimester. Commonly the only treatment necessary is scaling and oral hygiene instruction. An epulis may require surgical removal.

Pericoronitis is inflammation of the soft tissues (operculum) surrounding the crown of a partially erupted tooth, caused by an infection and/or debris beneath the operculum. The most commonly involved teeth are the lower third molars. In many instances the swollen tissues become traumatized by opposing teeth, worsening the symptoms. Acute pericoronitis is associated with a range of symptoms including severe pain, trismus, swelling and fever. Flushing the area and at home oral hygiene is usually the only treatment required. Antibiotics may be prescribed for more severe infections or when there are signs of systemic involvement. Operculectomy or tooth removal is often indicated in cases of recurrent pericoronitis.

Acute herpetic gingivostomatitis is a primary infection caused by the herpes simplex virus (HSV-1, perhaps HSV-2). HSV-1 may have a long incubation period (≤26 days). Primary herpetic gingivostomatitis usually occurs during childhood but is often subclinical. It is characterized by a sudden onset, with symptoms that could include fever, malaise, headache, and cervical lymphadenopathy. Vesiculo-ulcerative eruptions may be seen on the skin around the mouth, vermilion border, or intra-oral mucosa. The diagnosis is commonly based on the clinical exam and case history only, but if undertaken, cytologic analysis may show characteristic giant cells called Tzank cells and/or eosinophilic inclusion (Lipshultz) bodies. If diagnosed early, antiviral therapy (Acyclovir, 15 mg/kg five times daily for 7 days) may be of benefit. The infection is expected to resolve within 10-14 days and palliative care is often the only treatment necessary..

Desquamative gingivitis is a clinical term describing the presence of painful desquamation/erosion, erythema (fiery red), and blistering of attached and marginal gingiva. It is more common in middle-aged to elderly females, and can be mistaken for plaque-induced gingivitis. For accurate diagnosis, a microscopic evaluation (biopsy) is required. Gingival desquamation may be the result of various disease processes, including:

mucous membrane pemphigoid (MMP).
oral lichen planus.
pemphigus vulgaris.
pemphigoid.
chronic ulcerative stomatitis.
lupus erythematosus.
linear IgA disease.
dermatitis herpetiformis.
erythema multiforme.

PATHOGENESIS OF PERIODONTITIS

Periodontitis is an inflammatory disease of the periodontal structures which is characterized by the progressive destruction of the tissues supporting the tooth. The main clinical features of periodontitis include clinical attachment loss, alveolar bone loss, periodontal pocketing, and gingival inflammation. Gingival enlargement, gingival recession, gingival bleeding, increased mobility and tooth exfoliation may be seen. For periodontal disease to start and progress you need a susceptible host and periodontal pathogens. Periodontitis may be evident radiographically, but gingivitis is imperceptible on a radiograph. Histologically periodontal disease is marked by the apical migration of the junctional epithelium from the cemento-enamel junction (CEJ) and the formation of long junctional epithelium. There is a progressive degeneration in the adjacent connective tissue as the junctional epithelium proliferates along the root surface.

CYTOKINES AND CHEMOKINES

Cytokines are chemokines (secreted proteins) responsible for cell-to-cell signaling. Bacterial metabolic byproducts activate the patient’s innate immune system to release pro-inflammatory cytokines. Monocytes/macrophages are very important for regulating the immune response through the release of these chemical mediators, and a hyper-inflammatory monocyte/macrophage phenotype can lead to a hyper-reactive inflammatory response. Cytokines activate the acquired immune system leading to further progression of damage to the periodontal ligaments, gingiva, and alveolar bone. These proteins can cause an overproduction of collagenase increasing the breakdown of connective tissue. There are many inflammatory cytokines and chemokines identified to be associated with periodontal disease:

Interleukin – IL-1α, IL-1β, IL-4, IL-6, IL-8, IL-10, IL-12, IL-17.

- IL-1 – associated with bone resorption (osteoclast proliferation).
- IL-8 – important for chemotaxis.

Prostaglandins (PE2).

- Synthesized from fatty acids (arachidonic acid of cell membranes) in response to cyclo-oxygenases (COX-1 and COX-2).
- COX-2 is upregulated by IL-1, TNF, and bacterial lipopolysaccharide (LPS).
- Can be inhibited by nonsteroidal anti-inflammatory drugs (aspirin, ibuprofen etc.).

Bradykinin – inflammatory peptide that causes arteriole dilation and veno-constriction, leading to capillary bed leakage. Angiotensin Converting Enzyme inhibitors (ACE inhibitors) increase bradykinin levels which increases its blood pressure lowering effect.

Tumor necrosis factor (TNFα) – important for bone resorption and macrophage activation.

Other important cytokines include Interferon-γ, induced protein (IP)-10, and macrophage colony-stimulating factor. Leukocytes, especially PMNs, appear to have specialized receptors for a host of chemotactic agents, including C5a, TNF, IL-1, IL-8, LtB4, and IFN-g.

THE COMPLEMENT SYSTEM

The complement system is a part of the innate immune system, important in many of the body’s defense mechanisms. Complement enhances the antibody response, assists opsonization and phagocytosis, promotes inflammation, and directly attacks pathogens or compromised cells. The complement system consists of around 50 proteins which are mostly synthesized by hepatocytes in the liver, though other cells (macrophages, monocytes, epithelial cells etc) contribute. Proteases in the system are important for initiating a cascading response by cleaving specific proteins to release cytokines. Proteins associated with the complement system make up about 10% of the globulin fraction of blood serum. C3b has the ability to adhere to bacteria and enhance opsonization, the immune process where opsonins “tag” foreign pathogens for elimination by phagocytosis. C3a and C5a also induce the release of histamine and serotonin from neighboring mast cells. Three biochemical pathways activate the complement system:

Classical complement pathway – initiated by antigen-antibody complexes (IgG, IgM). Activation is followed by a series of enzyme-mediated reactions that result in the production of C5 and the assembly of the membrane attack complex (MAC). The former attracts and activates phagocytes, the latter creates a tunnel in the cell’s membrane that induces cell lysis and death.

Alternative complement pathway – the most common method of activation that also leads to the formation of the membrane attack complex. This pathway is commonly triggered when C3b directly binds a microbe, but can also be initiated by foreign materials or injured tissues.

Lectin pathway – initiated by mannose-binding lectin (MBL) or ficolin binding to certain sugars. The structure of the lectin pathway is similar to the classical complement pathway. Activation of C4 and C2 produces activated complement proteins further down the cascade.

Matrix metalloproteinase (MMP) is perhaps the most important proteinase associated with the destruction of periodontal tissues. MMPs are found in most cells, but polymorphonuclear leukocytes are known to produce large quantities of MMP-8 (collagenase), as well as oxygen radicals which are toxic to cells of the periodontium. MMP-1 is associated with resident fibroblasts, monocytes/macrophages, and epithelial cells. Some periodontal bacteria such as Porphymonas gingivalis and Aggregatibacter actinomycetemcomitans (Aa) are known to produce MMPs.

Endotoxins are large molecules (Lipopolysaccharides) located in the cell wall of gram-negative bacteria. Often detected in dental plaque, endotoxins have significant pathogenic potential and are capable of promoting bone resorption, inhibiting osteogenesis, attracting neutrophils, inducing tissue inflammation, activating complement pathways, and stimulating macrophages. Endotoxin is an important factor in the pathogenesis of periodontal disease.

Gonadotropins are hormones secreted by gonadotropic cells of the anterior pituitary gland. Gonadotropin expression is regulated by gonadotropin-releasing hormone (GnRH) from the hypothalamus. Examples of gonadotropins include follicle-stimulating hormone, luteinizing hormone, and human chorionic gonadotropin (hCG). Hormonal changes associated with puberty, menstruation, pregnancy, oral contraceptive use, and menopause can have in impact on periodontal tissues. Hormonal modifiers alter the host response but do not directly cause periodontal disease.

Luteinizing hormone (LH) is primarily associated with the stimulation of the Leydig cells of the testes and the theca cells of the ovaries to produce testosterone (and subsequently estradiol). Follicle-stimulating hormone (FSH) stimulates the production of estrogen by the ovaries. During the first trimester of pregnancy increasing levels of circulating hCG stimulate the production of estrogen and progesterone. An increase in gonadotropic hormones like estradiol and progesterone may lead to increased levels of Prevotella intermedia and Capnocytophaga species in the bacterial plaque, likely due to these hormones acting as a menadione (growth factor) substitute. Immune suppression during pregnancy may also contribute to the increased susceptibility to gingivitis/periodontitis.

Halitosis (bad breath) is primarily caused by proteolytic enzymes from gram-negative anaerobic bacteria that produce foul-smelling volatile sulfide compounds (VSCs).

CLASSIFICATION OF PERIODONTITIS

Previous classifications of periodontitis were based on the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. Substantial new information has emerged from population studies, basic scientific investigations, and the evidence from prospective studies evaluating environmental and systemic risk factors of periodontal disease. The analysis of this evidence has prompted the 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions to reclassify periodontitis.

This new classification has superseded older classifications. However, it may be wise to remain familiar with the older classification categories. The health of the patient’s periodontium may be assessed directly, from visible gingival inflammation (changes in appearance) and levels of plaque and calculus buildup. In health, the level of the free gingival margin should rest about 2-3mm coronal to the cemento-enamel junction (CEJ), and the epithelial attachment is found at or immediately adjacent to the CEJ. In health, the alveolar bone crest lies 1-2mm below the level of the CEJ. The distance between the start of the epithelial attachment and the crest of the alveolar bone is known as the biological width. The new periodontal classification system is broken down as the following:

1. Necrotizing Periodontal Diseases.

Necrotizing Gingivitis.
Necrotizing Periodontitis.
Necrotizing Stomatitis.

2. Periodontitis as Manifestation of Systemic Diseases.

3. Periodontitis.

STAGE – based on the severity and extent of distribution, as well as the complexity of management. “Stage” is a snapshot in time. Severity is primarily based on the interdental clinical attachment loss (CAL) at the worst site. Complexity is primarily based on additional local factors (furcation involvement, trauma, bite collapse etc.)

- - Stage I – Initial periodontitis

- - - - 1-2mm CAL
      - ≤4mm probing depth
      - mostly horizontal bone loss
      - no teeth lost

- - Stage II – Moderate periodontitis

- - - - 3-4mm CAL
      - ≤5mm probing depth
      - mostly horizontal bone loss
      - no teeth lost

- - Stage III – Severe periodontitis with the potential for additional tooth loss

- - - - +5mm CAL
      - ≥6mm probing depth
      - ≥3mm vertical bone loss
      - furcation involvement Class II or greater
      - ≤4 teeth lost

- - Stage IV – Severe periodontitis with the potential for loss of the dentition

- - - - +5mm CAL
      - ≥6mm probing depth
      - ≥3mm vertical bone loss
      - furcation involvement Class II or greater
      - Occlusal trauma
      - Occlusal collapse, drifting, or flaring
      - ≥5 teeth lost, or ≤20 teeth remaining.

EXTENT (distribution).

- - Localized – less than 30% of remaining teeth affected.
  - Generalized – more than 30% or remaining teeth affected.
  - Molar-incisor distribution.

GRADE – determined by the rate of progression, responsiveness to treatment, and the assessment of risk. Unlike staging, the grade is a dynamic measurement of how things are changing over time.

- - Grade A – Slow rate of progression.

- - - - No CAL in the past 5 years
      - %RBL/Age – less than 0.25
      - Minimal bone loss despite plaque buildup
      - Non-smoker
      - No diabetes
      - C-reactive protein less than 1mg/L

- - Grade B – Moderate rate of progression.

- - - - ≤2mm CAL in the past 5 years
      - %RBL/Age – between 0.25 and 1.0
      - Bone loss consistent with plaque buildup
      - Smoker (less than 10 cigarettes per day)
      - Well controlled diabetes
      - C-reactive protein 1-3mg/L

- - Grade C – Rapid rate of progression.

- - - - ≥2mm CAL in the past 5 years
      - %RBL/Age – more than 1.0
      - Excessive bone loss in light of plaque buildup
      - Smoker (more than 10 cigarettes per day)
      - Poorly controlled diabetes
      - C-reactive protein more than 3mg/L

PREVIOUS CLASSIFICATIONS OF PERIODONTAL DISEASE

An age dependent classification of periodontal disease (adult periodontitis, juvenile periodontitis, early-onset periodontitis etc.) has largely been replaced by classification according to the clinical, radiographic, historical, and laboratory findings.

Aggressive periodontitis is an older classification of a destructive disease characterized by:

the involvement of multiple teeth.
a distinctive pattern of rapid attachment loss and bone destruction.
an early age of onset.
the absence of systemic diseases (otherwise healthy patients).
hyperresponsive macrophages, producing increased prostaglandin E2 (PGE2) and interleukin-1.

Aggressive periodontitis can be further classified according to its distribution:

Generalized form of aggressive periodontitis – usually occurs between 12 and 25 years of age and is characterized by rapid, severe destruction of the periodontal structures around most teeth. Episodic, rapid and severe attachment loss is seen. The generalized form is associated with a weak serum response and is most strongly associated with Prevotella intermedia and Eikenella corrodens.

Localized form of aggressive periodontitis – usually occurs between 8 and 22 years of age and is characterized by rapid, severe destruction of the periodontal structures around the incisors and first molars. There may be a relative lack of local factors (plaque) to explain the destruction. The localized form is associated with a strong serum response and is most strongly associated with gram-negative anaerobes Actinobacillus Actinomycetemcomitans and Capnocytophaga species. Prevotella intermedia and Eikenella corrodens are present but to a lesser extent.

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