Inflammation When inflammation occurs a healthy gingiva develops gingivitis (due to presence of plaque deposits) and later on it progresses

to periodontitis according to certain thresholds, bacteria or deposits.

Healthy gingiva

Gingivitis

Periodontitis

Regarding pathogenesis, most of the damage happens to the host tissues because of the immune response. Immune responses are categorized as either innate (provides an immediate but non-specific response) or adaptive system (adapts the response to a specific pathogen).

What is inflammation? It is an observable alteration in tissues associated with changes in vascular permeability and dilation, often with the infiltration of leukocytes into affected tissues. It is considered one of the first responses. Inflammation is divided into two categories acute and chronic inflammation. Immediately after I get any injury I will get an acute inflammation (cuts, wounds), we will talk about chemical and physical defense later. The immune response in acute inflammation differs than that of chronic inflammation. We have three outcomes of acute inflammation, I might go from acute inflammation to abscesses of the periodontium (dental abscesses in general), and I could go from acute to chronic inflammation or resolution.

Injury
Acute Inflammation

Abcsesses of the periodontum

Chronic Inflammation

Resolution

Inflame is to set a fire, and inflammation is considered the dynamic response for vascularized tissues. I dont get an inflammation in dentin, enamel or cementum because they dont have a vascular system, so inflammation is the protective response of vascularized tissues to the injury. The vascular and cellular responses of inflammation are mediated by chemical factors (derived from blood plasma or some cells) and triggered by inflammatory stimulus. Tissue injury or cell death releases mediators. Irritants could be microbiological, physical, chemical or biological.

Inflammation | Periodontics II

 Cardinal signs of inflammation: 1. Redness (Hyperemia) 2. Warm (Hyperemia) because of the increase in blood flow in the area. 3. Pain (Nerve endings, Chemical mediators). 4. Swelling (Exudation) because fluids leave the vascular system and go to the tissues. 5. Loss of function because of pain.

This is the normal vascular system, the arterial part and the venous part. This is when I have inflammation, look at the macrophages and the neutrophils. Vasodilation will take place, then exudation and Edema, after that Emigration of cells and Chemotaxis.

Healthy Gingiva

How do I know whether this gingiva is inflamed or healthy? Color: Healthy gingiva usually has a color that has been described as "coral pink." Other colors like red, white, and blue can signify inflammation (gingivitis) or pathology. Although described as the color coral pink, variation in color is possible. This can be the result of factors such as: thickness and degree of keratinization of the epithelium, blood flow to the gingiva, natural pigmentation, disease and medications.
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Contour: Healthy gingiva has a smooth scalloped appearance around each tooth. Healthy gingiva fills and fits each interdental space, unlike the swollen gingiva papilla seen in gingivitis or the empty interdental embrasure seen in periodontal disease. Healthy gums hold tight to each tooth in that the gingival surface narrows to "knifeedge" thin at the free gingival margin. On the other hand, inflamed gums have a "puffy" or "rolled" margin. Texture: Healthy gingiva has a firm texture that is resistant to movement, and the surface texture often exhibits surface stippling. Unhealthy gingiva, on the other hand, is often swollen and less firm. Healthy gingiva has an orange-peel like texture to it due to the stippling. Reaction to disturbance: Healthy gums usually have no reaction to normal disturbance such as brushing or periodontal probing. Unhealthy gums on the other hand will show bleeding on probing (BOP). Wikipedia.

Stippling is found in around 50-70 % of the cases.

Stages of periodontal diseases 1. 2. 3. 4. Stage 1: Initial stage. Stage 2: Early stage. Stage 3: Established stage. Stage 4: Advanced lesion

Gingivitis
Periodontitis

I have initial, early and established stages; those three stages are considered to be gingivitis. Periodontal diseases in general are categorized into two stages the first one is inflammation of the gingiva which is gingivitis, and the second one is periodontitis; the inflammation of the periodontium (cementum, PDL and bone) which are the supporting structures. The fourth stage which is the advanced lesion is considered to be periodontitis.

Some students are confused between the initial and the early stages. The initial stage is the starting stage, but the early stage already started.

Inflammation | Periodontics II

Initial lesion The cause of all periodontal diseases is plaque (biofilm). The initial stage is considered to be subclinical gingivitis, so theres no BOP or edema. There are 2-4 days of accumulation of plaque on the sulcus, so there will be changes in the junctional epithelium and the perivascular connective tissue, increase in the number of capillaries and the dimension of the plexus, and an increased migration of leukocytes (Polymorphonuclear leukocytes). Now remember that the innate system works before the adaptive system on the bacterial infection or any problem. PMNs are secreted and they are the type of cells which dominate in this stage. Extravasation takes place; PMNs start rolling and they leave the vascular system (migration) because of the chemotaxis. Plaque is formed on the cervical third. In 24 hours changes occur in the dentinogingival plexus. The hydrostatic pressure increases because of the dilations of capillaries, the exudate and the flow of GCF increase. Early lesion

Early lesion is when the clinical signs start showing (within 4-5 days). The dentinogingival plexus dilates and increases in number, the PMN migrates to the perio pocket and phagosytosis of bacteria causes redness in the marginal gingiva (erythema) and BOP. Lymphocytes and PMNs predominate.

Collagen fibers are damaged by collagenase, because of infiltration of the PMNs in the area, these collagen fibers (circular and dento-gingival fiber groups) are closing it, and so PMNs leave the plexus from here and go towards the pocket, so I get 70% damage of collagen fibers. And that leads to leukocyte infiltration. Remember that collagen fibers -especially type 1- form most of the connective tissue of the gingiva. After that basal cells proliferate (junctional and sulcular epithelium) to increase the dimension of epithelium and number of cells in order to have enough barrier against the microbes, infections and toxins of bacteria. Rete pigs can be seen invading the coronal portion of the lesion in the connective tissue. In the oral epithelium I already have them, but in the coronal and sulcular epithelium I shouldnt have them. The coronal portion of the junctional epithelium is lost.
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Established lesion The established lesion is chronic gingivitis. I start having congested blood vessels, impaired venous return (the venous system closes the area, so I have more edema), extravasation of red blood cells which gives me the blue color and the GCF flow increases to compensate for the inflammatory response. The rete pigs extend deeper into the connective tissues. I have BOP. We have sulcular epithelium, junctional epithelium and oral epithelium, but theres another type of epithelium which is not normal (pocket epithelium): Not attached to the tooth surface Harbors large numbers of leukocytes Allows for further apical migration of the biofilm. When compared to the junctional epithelium, its more permeable and may be ulcerated.

Invasion for the bacteria and biofilm inside the connective tissue is very simple in this case. Advanced lesion There are two types of the established lesion: Remains stable for months or years. So gingivitis doesnt advance to periodontitis despite of the plaque and calculus accumulation. (11%) Becomes more active and converts more rapidly to destructive advanced lesion. So patient develops periodontitis. (30%) We still dont have enough information or data about when gingivitis advances into periodontitis and when it doesnt.

Advanced lesion: Loss of connective tissue attachment and alveolar bone, extensive damage to collagen fibers and the junctional epithelium migrates apically from the cemento enamel junction. Extravasation of leukocytes increases. Plasma cells dominate in this stage. Plasma cells originate from the B cells and they are from the adaptive immune response.
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Periodontal disease

Gingivitis Periodontal disease Periodontitis

Reversible tissue damage Irreversible tissue damage

Gingivitis is confined to the outer layer of gingival tissues. I dont have any problems on the radiograph, so its a reversible disease. The characters of gingivitis: Red or bluish red tissues. Swollen and rounded margins. Bulbous or swollen papillae. Bleeding upon gentle probing. Probing depth might be exceeding 3 mm because of swelling, over growth and edema (pseudo pocket). No apical migration of the junctional epithelium, its still in its normal place. No bone loss.

Let us have a look here at the difference of color; its obvious that the reddish color is the beginning of gingivitis. Here too, I have marginal slight redness, swelling, very shiny points, loss of stippling and loss of the scalloped feature of gingiva. Its very important to remember the anatomy of gingiva and teeth. Slight marginal redness - early gingivitis

Inflammation | Periodontics II

Marginal and papillary redness

Slight marginal and papillary redness

Red marginal gingiva and papillae

Blunted Papillae

Bulbous Papillae

Cratered Papillae

Here I have a blunted papilla, I want you to differentiate it from the cratered papilla, which you see in certain diseases like NUG (Necrotizing Ulcerative Gingivitis) and NUP (Necrotizing Ulcerative Periodontitis). Its also called punched out or plaque triangle because of losing the papilla in that area.

Soft spongy tissue

Smooth shiny tissue

The smooth and shiny tissues are also signs and symptoms of inflammation. Inflammation results in ulceration of the pocket wall. Bleeding on gentle probing is an important indicator of inflammation.

Inflammation | Periodontics II

Extent and Distribution of Inflammation

Diagnosis is giving the full name in order, so if I want to talk about the extension of inflammation, its either generalized or localized. Severity of gingivitis is not important, but if you want to use it you have to depend on the Gingival Index (mild, moderate or severe). After that I put the disease name (E.g., plaque induced gingivitis). You shouldnt write chronic gingivitis, theres nothing such as chronic gingivitis, it is either plaque induced or non-plaque induced. The distribution differs from the diagnosis. The distribution is what I write in the file (papillary, marginal, or diffuse). The distribution has nothing to do with diagnosis. Diagnosis = Extent + Severity + name of the disease. (E.g., Generalized Mild Plaque-induced Gingivitis)

Localized Diffuse

Generalized Diffuse

Localized Marginal

Diffuse

Inflammation | Periodontics II

Classification of gingival diseases I have plaque induced and non-plaque induced. That is according to the American academy of periodontology 1999. The plaque induced includes any gingival disease cause by the plaque.

Dental PlaqueInduced Gingival Disease 1. Gingivitis associated with dental plaque only (no orthodontic treatment or over hanged restoration). 2. Gingival diseases modified by systemic factors (E.g., epileptic patient) 3. Gingival diseases modified by medications 4. Gingival diseases modified by malnutrition If the patient has good oral hygiene and no plaque, he will not develop gingivitis. 1. Gingivitis associated with dental plaque only: A. without other local contributing factors B. with local contributing factors Most common form Plaque at gingival margin Redness, tenderness Swollen margins Bleeding on probing

With local factors

2. Gingival diseases with modifying factors: Three main categories of gingival diseases with modifying factors: Systemic factors Medications Malnutrition

Inflammation | Periodontics II

- Gingival Diseases Modified by Systemic Factors In this form of gingival disease, plaque initiates the disease. Then, specific systemic factors found in the host modify the disease process A. associated with the endocrine system (E.g., diabetes) B. associated with blood diseases

In the anterior maxilla mostly

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I usually have a normal response to plaque like slight inflammation, but here I have an exaggerated response because of hormonal imbalance.

Plaque accumulation is not necessary for initiation of gingival enlargement, but it will exacerbate the gingival disease. Meticulous plaque control can reduce but will not eliminate gingival overgrowth.

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Inflammation | Periodontics II

Anticonvulsant-Phenytoin induced

Gingival Enlargement Onset within 3 months of taking medication Exaggerated response to plaque Higher prevalence in children Gingiva on anterior sextants most commonly affected Enlargement first observed at the interdental papilla

Immunosuppressant-Cyclosporine induced

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Inflammation | Periodontics II

The treatment of all plaque induced gingival diseases is OHI. I could talk to the patient after the appointment or during the procedure while Im scaling, depending on his level of education. But for people who have poor knowledge about it I could use simple words. After that I start scaling supra-gingival and sub-gingival. Then I could give him an antimicrobial or antiseptic drug (not for all patients). The most important way to control plaque and prevent gingival and periodontal diseases is mechanical debridement, scaling and root planning. When do I give an antimicrobial agent? If the patient cannot reach the area, if he is very old or after the surgery I will prescribe chlorhexidine for 5 or 6 days.

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Inflammation | Periodontics II

When I say bacterial non-plaque induced, I mean that it is caused by a bacterium that is not common in gingival plaque (E.g., Neisseria). I have around 500 hundred species. Viral (herpes), Fungal (candida), Genetic (downs syndrome), Systemic condition (diabetes), Traumatic (cuts and wounds), Foreign bodies (chemicals).

Best of luck, Sarah Ahmed Al-Akhras.

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Inflammation | Periodontics II