CAUSES OF GINGIVAL RECESSION MCQ REVIEW

What  is Periodontal fremitus

Periodontal fremitus occurs in either of the alveolar bones when an individual sustains trauma from occlusion. It is a result of teeth exhibiting at least slight mobility rubbing against the adjacent walls of their sockets, the volume of which has been expanded ever so slightly by inflammatory responses, bone resorption or both. As a test to determine the severity of periodontal disease, a patient is told to close his or her mouth into maximum intercuspation and is asked to grind his or her teeth ever so slightly. Fingers placed in the labial vestibule against the alveolar bone can detect fremitus.

A NOTE ON CLASSIFICATION, CLINICAL FEATURES, PATHOGENESIS OF PERIODONTAL POCKET

The periodontal pocket, defined as a pathologically deepened gingival sulcus, is one of the most important clinical features of periodontal disease. All different types of periodontitis share histopathologic features such as tissue changes in the periodontal pocket, mechanisms of tissue destruction, and healing mechanisms. They differ, however, in their etiology, natural history, progression, and response to therapy.

CLASSIFICATION

Deepening of the gingival sulcus may occur by coronal movement of the gingival margin, apical displacement of the gingival attachment, or a combination of the two processes.

Illustration of pocket formation indicating expansion in two directions (arrows) from the normal gingival sulcus (left) to the periodontal pocket (right)

Different types of periodontal pockets. A, Gingival pocket. There is no destruction of the supporting periodontal tissues. B, Suprabony pocket. The base of the pocket is coronal to the level of the underlying bone. Bone loss is horizontal. C, Intrabony pocket. The base of the pocket is apical to the level of the adjacent bone. Bone loss is vertical.

Pockets can be classified as follows:

Gingival pocket (pseudo pocket):

This type of pocket is formed by gingival enlargement without destruction of the underlying periodontal tissues. The sulcus is deepened because of the increased bulk of the gingiva

Periodontal pocket:

This type of pocket occurs with destruction of the supporting periodontal tissues. Progressive pocket deepening leads to destruction of the supporting periodontal tissues and loosening and exfoliation of the teeth.

Two types of periodontal pockets exist:

Suprabony (supracrestal or supraalveolar), in which the bottom of the pocket is coronal to the underlying alveolar bone.

Intrabony (infrabony, subcrestal or intraalveolar), in which the bottom of the pocket is apical to the level of the adjacent alveolar bone. In this second type, the lateral pocket wall lies between the tooth surface and the alveolar bone.

Pockets can involve one, two, or more tooth surfaces and can be of different depths and types on different surfaces of the same tooth and on approximating surfaces of the same interdental space . Pockets can also be spiral (i.e., originating on one tooth surface and twisting around the tooth to involve one or more additional surfaces). These types of pockets are most common in furcation areas.

Classification of pockets according to involved tooth surfaces. A, Simple pocket. B, Compound pocket. C, Complex pocket

CLINICAL FEATURES

Clinical signs such as bluish-red, thickened marginal gingiva;

A bluish-red vertical zone from the gingival margin to the alveolar mucosa;

Gingival bleeding, suppuration,or both;

Tooth mobility;

And diastema formation and symptoms such as localized pain or pain "deep in the bone" are suggestive of the presence of periodontal pockets.

The only reliable method of locating periodontal pockets and determining their extent is careful probing of the gingival margin along each tooth surface.

A, Extrusion of the central incisor and diastema associated with the periodontal pocket. B, The entire length of the periodontal probe inserted to the base of the periodontal pocket in the central incisor

Correlation of Clinical and Histopathologic Features of the Periodontal Pocket
Clinical Features	Histopathologic Features
1. The gingival wall of the periodontal pocket presents various degrees of bluish-red discoloration; flaccidity; a smooth, shiny surface; and pitting on pressure.	1. The discoloration is caused by circulatory stagnation; the flaccidity, by destruction of the gingival fibers and surrounding tissues; the smooth, shiny surface, by the atrophy of the epithelium and edema; the pitting on pressure, by edema and degeneration.
2. Less frequently, the gingival wall may be pink and firm.	2. In such cases, fibrotic changes predominate over exudation and degeneration, particularly in relation to the outer surface of the pocket wall. However, despite the external appearance of health, the inner wall of the pocket invariably presents some degeneration and is often ulcerated.
3. Bleeding is elicited by gently probing the soft tissue wall of the pocket.	3. Ease of bleeding results from increased vascularity, thinning and degeneration of the epithelium, and the proximity of the engorged vessels to the inner surface.
4. When explored with a probe, the inner aspect of the periodontal pocket is generally painful.	4. Pain on tactile stimulation is due to ulceration of the inner aspect of the pocket wall.
5. In many cases, pus may be expressed by applying digital pressure.	5. Pus occurs in pockets with suppurative inflammation of the inner wall.

On the basis of depth alone, however, it is sometimes difficult to differentiate between a deep normal sulcus and a shallow periodontal pocket. In such borderline cases, pathologic changes in the gingival distinguish the two conditions.

PATHOGENESIS

The initial lesion in the development ofperiodontitis is the inflammation of the gingiva in response to a bacterial challenge. Changes involved in the transition from the normal gingival sulcus to the pathologic periodontal pocket are associated with different proportions of bacterial cells in dental plaque. Healthy gingiva is associated with few microorganisms, mostly coccoid cells and straight rods. Diseased gingiva is associated with increased numbers of spirochetes and motile rods. However, the microbiota of diseased sites cannot be used as a predictor of future attachment or bone loss because their presence alone is not sufficient for disease to start or progress.

Extension of the junctional epithelium along the root requires the presence of healthy epithelial cells. Marked degeneration or necrosis of the junctional epithelium retards rather than accelerates pocket formation. Degenerative changes seen in the junctional epithelium at the base of periodontal pockets are usually less severe than those in the epithelium of the lateral pocket wall. Because migration of the junctional epithelium requires healthy, viable cells, it is reasonable to assume that the degenerative changes seen in this area occur after the junctional epithelium reaches its position on the cementum.

The transformation of a gingival sulcus into a periodontal pocket creates an area where plaque removal becomes impossible, and the following feedback mechanism is established:

The rationale for pocket reduction is based on the need to eliminate areas of plaque accumulation.

A NOTE ON DENTAL CALCULUS

Dental calculus

For the periodontal diseases:

•     The primary etiologic factor is: Is the dental plaque.
•       The associated factor: is the dental calculus, it helps in new formation of the plaque.
•       The modifying factor: is a systemic disease, it aggravates the disease when the plaque is presents.

 Calculus:

•    Is a mineralized dental plaque that occurs in the tooth surfaces & dental prosthesis, it has many forms:
•    Bridging over the gingival margin.
•     Follow the festooning shape of the dentition.
•     Lobular form.
•     In case of malalignment :àprotected area for the plaque à calculus

 Classification:

             Supragingival                  &               subgingival calculus..

         Generally: both can occur together or one may appear alone.

Subgingival calculus: 

•      Gingival fluid origin.
•       Below the crest of the gingival margin.
•       Hard, dark& flint like.
•       Greenish black or dark brown in color.
•       Firmly attached to the tooth, can’t be seen and detected by explorer No.621 probe.
•       Extent nearly to the base of the pocket in chronic periodntitis, but doesn’t reach the Junctional epithelium.

 Supragingival calculus:    

•     Saliva origin.
•    Coronal to the gingival margin. Can be composed of supra &sub gingival calculus.
•    Hard, clay like consistency, White, white yellowish in color& its color may be affected by the tobacco or food stain.
•     Easy to be seen in the oral cavity, may be generalized or localized.
•     Easy to be removed &usually recurrent especially in the: Lower incisors. 

• Most common location :near to the orifices of the S. glands’ ducts

Parotid gland’s duct ”stenson”----->opposite to buccal surface of maxillary molars.

Submandibular “bartholine” & sublingual “wharton” ducts ----->Lingual surface of lower incisors.

it’s shape : either covers the occlusal surfaces or  bridge like structure over interdental papilla.

                                                Calculus contents:

Inorganic contents:70-90%		Organic contents
2/3 of the calculus inorganic component is in crystalline form ;there are  4 types of crystals . The crystals are: hydroxyappatite ,58% à magnesium white locate,21%  àmost in post octacalcium phosphate,12% Brushite, 9% àmost in mandibular anteriors. Detected more frequently in supragingival calculus. Constitute the bulk. Generally 2 or more crystals are detected in the calculus. Incidence of 4 crystals à varies with age of calculus.		Mixture of  : Protein-poly saccharide complex + desquamated host cells (leukocytes & host cells) + microorganisms. Carbohydrates (1.9-9.1%): Glucose , glactose   ,mannose ,arabinose ,rhamnose glucoric acid ,glactouric acid glucoseamine & glactose amine. à all are present in saliva except : Rhaminose  &  arabinose . Salivary proteins (5.9-8.2%): Most are amino acids. lipids 0.2%:nutral fat ,fatty acids ,cholesterol ester, phospholipids & cholesterol.
*Contents:	The differences     Supra gingival calculus	Between: Sub gingival calculus
hydroxyappatite: Ca Ph : Mg white: brushite: ratio of Ca/Ph: sodium contents: salivary proteins:	Equal.   More. Less. More. Low.   Increase with the depth of PD pocket. Yes	Equal Less. More Less. Higher. No.

Calculocementum:

Is the calculus has morphological appearance similar to cementum. This is because the calculus is interdigitates the cementum & no differences between them.

Mode of attachment of the calculus to the tooth surface:

• Close adaptation under surface depression.
• In sub gingival calculus.
• By organic pellicle (very weak)
• Penetration of the bacteria to the cementum.
• Mechanical interlocking to the surface irregularities: resorption lacuna or caries, in the cementum by sharpies fibers.                          

Calculus formation:

Calculus is the dental plaque that undergoes mineralization.

Calcification starts                      4-8 hrs   after plaque.

50 % become mineralized after   2 days.

60-90                                          12 days.

• Plaque can be daily removed at home by brushing but the calculus is
• not ,it is only removed clinically by the dentist .

• Calculus formation à the bacterial action will stopped (adv) but it will act as stagnation area for new plaque accumulationà (protection for plaque). 

• Early plaque contains small amount of inorganic material but it will increase as the plaque develops into calculus. 

• All plaque doesn’t necessarily undergo calcification.

• It reaches a plateau of maximal mineral by 2 days.

• Microorganisms are not always essential in calculus formation. 

• Plaque has ability to conc. The Ca at  2-20 times it’s level in saliva. 

• There is a suggestion that Ph is more critical than Ca in plaque mineralization.

• Early plaque of heavy former àmore Ca ,3 times Ph &less K than non calculus former.

An Illustrative Note & PowerPoint presentation on Cementum

PERIODONTIUM

PERIODONTIUM

TEETH IN-SITU

Periodontium (forms a specialized fibrous joint called Gomphosis)

•         Cementum

•         Periodontal Ligament

•         Alveolar bone

•         Gingiva facing the tooth

Histology of periodontium

Cementum

It is a hard avascular connective tissue that covers the roots of teeth

Role of Cementum

1.    It covers and protects the root dentin (covers the opening of dentinal tubules)

2.    It provides attachment of the periodontal fibers

3.    It reverses tooth resorption

Varies in thickness:  thickest in the apex and In the inter-radicular areas of multirooted teeth, and thinnest in the cervical area 10 to 15 mm in the cervical areas to 50 to 200 mm (can exceed > 600 mm) apically

        
Cementum simulates bone

•          Organic fibrous framework, ground substance, crystal type, development

•          Lacunae

•          Canaliculi

•          Cellular component

•          Incremental lines (also known as “resting”  lines; they are  produced by continuous but            phasic, deposition of cementum)

Differences between cementum and bone

•         Not vascularized – a reason for it being resistant to resorption

•          Minor ability to remodel

•          More resistant to resorption compared to bone

•          Lacks neural component – so no pain

•          70% of bone is made by inorganic salts (cementum only 45-50%)

•          2 unique cementum molecules: Cementum attachment protein (CAP) and IGF

Clinical Correlation

Cementum is more resistant to resorption: Important in permitting orthodontic tooth movement

Development of Cementum

• Cementum formation occurs along the entire tooth
• Hertwig’s epithelial root sheath (HERS) –Extension of the inner and outer dentalepithelium
• HERS sends inductive signal to ectomesenchymal pulp cells to secrete predentin by differentiating into odontoblasts
• HERS becomes interrupted
• Ectomesenchymal cells from the inner portion of the dental follicle come in with predentin by differentiating into cementoblasts
• Cementoblasts lay down cementum 

PowerPoint presentation on Cementum

A NOTE ON DISEASES CLINICALLY PRESENTING AS DESQUAMATIVE GINGIVITIS

DISEASES CLINICALLY PRESENTING AS DESQUAMATIVE GINGIVITIS

Lichen Planus

Lichen planus is a relatively common, chronic, dermatosis characterized by the presence of cutaneous   violaceous papules that may coalesce to form plaques. The current evidence suggests that lichen planus is an immunologically mediated mucocutaneous disorder where host T lymphocytes play a central role . Although the oral cavity may present lichen planus lesions with a distinct clinical configuration and distribution, the clinical presentation sometimes may simulate other mucocutaneous disorders. Therefore a clinical diagnosis of oral lichen planus should be accompanied by a broad differential diagnosis. Numerous epidemiologic studies have shown that oral lichen planus presents in 0.1% to 4% of the population." The majority of patients with oral lichen planus are middle-aged and older females with a 2:1 ratio of females to males. Although possible, children are rarely affected. In a dental setting, cutaneous lichen planus is observed in about one third of the patients diagnosed with oral lichen planus.  In contrast, two thirds of patients seen in dermatologic clinics exhibit oral lichen planus.

Oral Lesions

Although there are several clinical forms of oral lichen planus (reticular, patch, atrophic, erosive and bullous), the most common are the reticular and erosive subtypes. The typical reticular lesions are asymptomatic, bilateral, and consist of interlacing white lines on the posterior region of the buccal mucosa. The lateral border and dorsum of the tongue, hard palate, alveolar ridge, and gingiva may also be affected. In addition, it is not unusual for the reticular lesions to have an erythematous background, a feature that is associated with the coexistence of candidiasis. Oral lichen planus lesions follow a chronic course and have alternating, unpredictable periods of quiescence and flares.

The erosive subtype of lichen planus is often associated with pain and clinically manifests as atrophic, erythematous areas. Fine white radiating striations are observed bordering the atrophic zones. These areas may be sensitive to heat, acid, and spicy foods.

Gingival Lesions

Up to 10% of patients with oral lichen planus have lesions restricted to the gingival tissue that may occur as one or more types of four distinctive patterns:

1. Keratotic lesions. These raised white lesions may present as groups of individual papules, linear or reticulate lesions, or plaquelike configurations.

2. Erosive or ulcerative lesions. These extensive erythematous areas with a patchy distribution may present as focal or diffuse hemorrhagic areas. These lesions are exacerbated by slight trauma (e.g., toothbrushing).

3. Vesicular or bullous lesions. These raised, fluid-filled lesions are uncommon and short lived on the gingiva, quickly rupturing and leaving an ulceration.

4. Atrophic lesions. Atrophy of the gingival tissues with ensuing epithelial thinning results in erythema confined to the gingiva.

Histopathologic, Direct, and Indirect Immunofluorescence Findings in Selected Conditions That May Present Clinically as Desquamative Gingivitis
Disease	Histopathology	Direct Immunofluorescence		Indirect Immunofluorescence
		Biopsy Perilesional Mucosa	Biopsy Uninvolved Mucosa
Pemphigus	Intraepithelial clefting above the basal cell layer. The basal cells have a characteristic "tombstone" appear- ance. Acantholysis is present.	Intercellular deposits in epithelium; IgG in all cases, C3 in most cases.	Same as perilesional mucosa.	Intercellular (IgG) anti- bodies in >90% of cases.
Cicatricial pemphigoid	Subepithelial clefting with epithelial separation from the underlying lamina propria, leaving an intact basal layer.	Linear deposits of C3, with or without IgG at the basement membrane zone in almost all cases.	Same as perilesional mucosa.	Basement membrane zone (IgG) antibodies in 10% of cases.
Bullous pemphigoid	Subepithelial clefting with epithelial separa- tion from the under- lying lamina propria, leaving an intact basal layer.	Linear deposits of C3, with or without IgG at the basement membrane zone in almost all cases.	Same as perilesional mucosa.	Basement membrane zone (IgG) antibodies in 40% to 70% of cases.
Epidermolysis bullosa acquisita	Similar to bullous and cicatricial pemphigoid.	Linear deposits of IgG and C3 at the Basement membrane zone in almost all cases.	Same as perilesional mucosa.	Basement membrane zone (IgG) antibodies in 25% of cases.
Lichen planus	Hyperkeratosis, hydropic degeneration of the basal layer, "saw-toothed" rete pegs. The lamina propria exhibits a dense, band- like infiltrate primarily of T lymphocytes. Colloid bodies are present.	Fibrilar deposits of fibrin at the dermal-epiderma junction.	Negative	Negative
Chronic ulcerative stomatitis	Similar to erosive lichen planus (hype rkeratosis, acanthosis, basal cell layer liquefaction, sub- epithelial clefting, and lympho-histiocytic chronic infiltrate in a bandlike configuration.	IgG deposits in nuclei of basal layer epithelial cells.	Same as perilesional mucosa.	ANA specific for basal cells of stratified squamous epithelium.
Linear IgA disease	Similar to erosive lichen planus.	Linear deposits of IgA at the basement membrane zone.	Same as perilesional mucosa.	IgA basement membrane zone (IgA) antibodies in 30% of cases.
Dermatitis herpetiformis	Collection of neutro- phils, eosinophils, and fibrin in connective tissue papillae.	IgA deposits in dermal papillae in 85% of cases.	IgA deposits in dermal papillae in 100% of cases.	IgA endomysial antibodies in 70% of cases, gliadin antibodies in 30% of cases.
Systemic lupus erythematosus	Hyperkeratosis, basal cell degeneration, epithelial atrophy, and perivascular inflammation.	I g (G or M), with or without C3 deposits at dermal-epidermal junction.	Same as perilesional mucosa.	ANA in more than 95% of cases, DNA and ENA antibodies in more than 50% of cases.
Chronic cutaneous lupus erythematosus	Hyperkeratosis, basal cell degeneration, epithelial atrophy, and perivascular inflammation.	Ig (G or M), with or without C3 deposits at dermal-epidermal junction.	Negative	Usually negative
Subacute lupus erythematosus	Less inflammatory cell infiltrate than systemic and chronic cutaneous lupus erythematosus but with similar microscopic features.	Ig (G or M), with or without C3 deposits at dermal-epidermal junction in 60% of cases; granular IgG deposits in basal cell cytoplasm in 30% of cases.	Same as perilesional mucosa.	ANA in 60% to 90%, SS-A(Ro) in 80%, RF in 30%, and RNP in 10% of cases.

Gingivitis: clinical features. A, Localized, diffuse, intensely red area facial of tooth #7 and dark pink marginal changes in the remaining anterior teeth. B, Generalized papillary gingivitis. C, Generalized marginal inflammatory lesion. D, Generalized diffuse inflammatory lesion. E, Papillary gingival enlargement. F, Different degrees of recession. Recession is slight in teeth #26 and 29 and marked in #27 and 28.

Note the irregular contours of the gingiva in #28 and the lack of attached gingiva in #27. G, Insertion of a probe into the gingival sulcus.

Note the lack of stippling, the slightly rolled margins, and the dark red color. H, Bleeding appears about 30 seconds after probing.

A, Necrotizing ulcerative gingivitis: typical punched out interdental papilla between mandibular canine and lateral incisor. B, Necrotizing ulcerative gingivitis: typical lesions with progressive tissue destruction. C, Necrotizing ulcerative gingivitis: typical lesions with spontaneous hemorrhage. D, Necrotizing ulcerative gingivitis: typical lesions producing irregular gingival contour. E, Primary herpetic gingivostomatitis: typical diffuse erythema. F, Primary herpetic gingivostomatitis: vesicles on the gingiva.

Erosive lichen planus presenting as desquamative gingivitis. The gingival tissues are erythematous, ulcerated, and painful.

Gingival mucous membrane pemphigoid. Lesions of cicatricial pemphigoid confined to the gingival tissues, producing a typical desquamative gingivitis appearance.

Pemphigus vulgaris of the gingiva. Clinical appearance of a patient with pemphigus vulgaris presenting oral lesions confined to the gingiva. The clinical diagnosis was consistent with desquamative gingivitis.

Pemphigus vulgaris of the oral cavity. Multiple and coalescent areas of ulceration covered by necrotic epithelium. This patient presented with large ulcers in the labial mucosa, tongue, and soft palate.

Chronic ulcerative stomatitis. Erythema and ulceration of the gingiva consistent with a clinical diagnosis of desquamative gingivitis.

Linear IgA. Intense erythema and ulceration of the gingiva consistent with desquamative gingivitis.

Lupus erythematosus of the oral cavity presenting as desquamative gingivitis. Intense erythema with ulceration bordered by white radial lines.

Plasma cell gingivitis. The gingiva presents a band of moderate to severe inflammation reminiscent of desquamative gingivitis.

Graft versus host disease in a recipient of an allogenic bone marrow transplant. The maxillary gingiva exhibits features consistent with desquamative gingivitis.

Wegener's granulomatosis affecting the gingi-val tissues. The classic "strawberry gums" appearance of the mandibular gingiva is seen in this patient. A slight resemblance with desquamative gingivitis is evident.

Erythema multiforme. Large, shallow, and painful ulcers involving the labial and buccal mucosae. Hemorrhagic crusting of the mandibular vermilion border of the lips is observed.

Treatment of lichen planus.

 Treatment of pemphigus vulgaris.

Treatment of cicatricial pemphigoid.