TECHNIQUES TO INCREASE ATTACHED GINGIVA (ROOT COVERAGE)

The following is a list of techniques used for gingival augmentation coronal to the recession (root coverage):

  1. Free gingival autograft
  2. Free connective tissue autograft
  3. Pedicle autografts: • Laterally (horizontally) positioned flap • Coronally positioned flap; includes semilunar pedicle (Tarnow)
  4. Subepithelial connective tissue graft (Langer)
  5. Guided tissue regeneration
  6. Pouch and tunnel technique

Subepithelial connective tissue graft (Langer) 🔎

Indication:

  • Larger and multiple defects with good vestibular depth and gingival thickness to allow a split-thickness flap to be elevated.

Adjacent to the denuded root surface, the donor connective tissue is sandwiched between the split flap as shown in the figure.

Subepithelial connective tissue graft for root coverage.
cont’d F to J, Facial views. F, Gingival recession. G, Vertical incisions to prepare recipient site. H, Split-thickness flap reflected. I, Connective tissue sutured over denuded root surface. J, Split-thickness flap sutured over donor connective tissue.

Surgical Technique Steps:

Step 1. Raise a partial-thickness flap with a horizontal incision 2 mm away from the tip of the papilla and two vertical incisions 1 to 2 mm away from the gingival margin of the adjoining teeth.

Step 2. Thoroughly plane the root, reducing its convexity.

Step 3. Obtain a connective tissue graft from the palate by means of a horizontal incision 5 to 6 mm from the gingival margin of molar and premolars. The connective tissue is carefully removed along with all adipose and glandular tissue. The palatal wound is sutured in a primary closure.

Step 4. Place the connective tissue on the denuded root. Suture it with resorbable sutured to the periosteum.

Step 5. Cover the graft with the outer portion of the partial-thickness flap and suture it interdentally.

Step 6. Cover the area with dry foil and surgical pack.

After 7 days, the dressing and sutures are removed. The esthetics are favorable with this technique since the donor tissue is connective tissue.

Dentowesome|@drmehnaz


Source: Carranza’s Clinical Periodontolgy, 10th Ed

INTRINSIC AND EXTRINSIC STAINS

Intrinsic Stains

Pre-eruptive Causes

These are incorporated into the deeper layers of enamel and dentin during odontogenesis and alter the development and appearance of the enamel and dentin

.Alkaptonuria: Dark brown pigmentation of primary teeth is commonly seen in alkaptonuria. It is an autosomal recessive disorder resulting into complete oxidation of tyrosine and phenylalanine causing increased level of homogentisic acid.

Hematological disorders

Erythroblastosis fetalis: It is a blood disorder of neonates due to Rh incompatibility. In this, stain does not involve teeth or portions of teeth developing after cessation of hemolysis shortly after birth. Stain is usually green, brown or bluish in color.

Congenital porphyria: It is an inborn error of por- phyrin metabolism, characterized by overproduction of uroporphyrin. Deciduous and permanent teeth may show a red or brownish discoloration. Under ultraviolet light, teeth show red fluorescence.

• Sickle cell anemia: It is inherited blood dyscrasia characterized by increased hemolysis of red blood cells. In sickle cell anemia infrequently the stains of the teeth are similar to those of erythroblastosis fetalis, but discoloration is more severe, involves both dentitions and does not resolve with time.

Amelogenesis imperfecta: It comprises of a group of conditions, that demonstrate developmental alteration in the structure of the enamel in the absence of a systemic disorders. Amelogenesis imperfecta (AI) has been classified mainly into hypoplastic, hypocalcified and hypomaturation type.

Fluorosis: In fluorosis, staining is due to excessive fluoride uptake during development of enamel. Excess fluoride induces a metabolic change in ameloblast and the resultant enamel has a defective matrix and an irregular, hypomineralized structure 

  • Vitamin D deficiency results in characteristic white patch hypoplasia in teeth.
  • Vitamin C deficiency together with vitamin A deficiency during formative periods of dentition resulting in pitting type appearance of teeth.
  • Childhood illnesses during odontogenesis, such as exanthematous fevers, malnutrition, metabolic disorder, etc. also affect teeth.
  1. Dentinogenesis imperfecta : It is an autosomal dominant development disturbance of the dentin which occurs along or in conjunction with amelogenesis imperfecta. Color of teeth in dentinogenesis imperfecta (DI) varies from gray to brownish violet to yellowish brown with a characteristic usual translucent or opalescent hue.
  2. Tetracycline and minocycline: Unsightly dis- coloration of both dentitions results from excessive intake of tetracycline and minocycline during the development of teeth. Chelation of tetracycline molecule with calcium in hydroxyapatite crystals forms tetracycline orthophosphate which is responsible for discolored teeth.

Posteruptive Causes

  • Pulpal changes: Pulp necrosis usually results from bacterial, mechanical or chemical irritation to pulp. In this disintegration products enter dentinal tubules and cause discoloration.
  • Trauma: Accidental injury to tooth can cause pulpal and enamel degenerative changes that may alter color of teeth.Pulpal hemorrhage leads to grayish discoloration and nonvital appearance. Injury causes hemorrhage which results in lysis of RBCs and liberation of iron sulfide which enter dentinal tubules and discolor surrounding tooth.
  • Dentin hypercalcification: Dentin hypercalcification results when there are excessive irregular elements in the pulp chamber and canal walls. It causes decrease in translucency and yellowish or yellow brown discoloration of the teeth.
  • Dental caries: In general, teeth present a discolored appearance around areas of bacterial stagnation and leaking restorations.
  • Restorative materials and dental procedures: Discoloration can also result from the use of endodontic sealers and restorative materials.
  • Aging: Color changes in teeth with age result from surface and subsurface changes. Age related discoloration are because of:– Enamel changes: Both thinning and texture changes occur in enamel.

Dentin deposition: Secondary and tertiary dentin deposits, pulp stones cause changes in the color of teeth.

Functional and parafunctional changes: Tooth wear may give a darker appearance to the teeth because of loss of tooth surface and exposure of dentin which is yellower and is susceptible to color changes by absorption of oral fluids and deposition of reparative dentin.

Extrinsic Stains

Daily Acquired Stains

Plaque: Pellicle and plaque on tooth surface gives rise to yellowish appearance of teeth.

Food and beverages: Tea, coffee, red wine, curry and colas if taken in excess cause discoloration.

Tobacco use results in brown to black appearance of teeth.

Poor oral hygiene manifests as:

  • –  Green stain
  • –  Brown stain
  • –  Orange stain.

Swimmer’s calculus:
– It is yellow to dark brown stain present on facial andlingual surfaces of anterior teeth. It occurs due toprolonged exposure to pool water.

Gingival hemorrhage.

Chemicals

• Chlorhexidine stain: The stains produced by use of chlorhexidine are yellowish brown to brownish in nature.

Metallic stains: These are caused by metals and metallic salts introduced into oral cavity in metal containing dust inhaled by industry workers or through orally administered drugs.

Stains caused by different metals

• Copper dust—green stain
• Iron dust—brown stain
• Mercury—greenish black stain • Nickel—green stain
• Silver—black stain.

Reference- Nisha garg textbook of endosontics and Anil Ghom textbook of oral medicine

GINGIVAL INFLAMMATION

Pathologic changes in gingivitis are associated with the presence of oral microorganisms attached to the tooth and perhaps in or near the gingival sulcus.

STAGE I GINGIVITIS: THE INITIAL LESION

The first manifestations of gingival inflammation are vascular changes consisting of dilated capillaries and increased blood flow. These initial inflammatory changes occur in response to microbial activation of resident leukocytes and the subsequent stimulation of endothelial cells. Clinically, this initial response of the gingiva to bacterial plaque is not apparent.

Changes can also be detected in the junctional epithelium and perivascular connective tissue at this early stage. For example, the perivascular connective tissue matrix becomes altered, and there is exudation and deposition of fibrin in the affected area. Also, lymphocytes soon begin to accumulate. The increase in the migration of leukocytes and their accumulation within the gingival sulcus may be correlated with an increase in the flow of gingival fluid into the sulcus.

The character and intensity of the host response determine whether this initial lesion resolves rapidly, with the restoration of the tissue to a normal state, or evolves into a chronic inflammatory lesion. If the latter occurs, an infiltrate of macrophages and lymphoid cells appears within a few days.

STAGE II GINGIVITIS: THE EARLY LESION

The early lesion evolves from the initial lesion within about 1 week after the beginning of plaque accumulation.Clinically, the early lesion may appear as early gingivitis, and it overlaps with and evolves from the initial lesion with no clear-cut dividing line. As time goes on, clinical signs of erythema may appear, mainly because of the proliferation of capillaries and increased formation of capillary loops between rete pegs or ridges . Bleeding on probing may also be evident.1 Gingival fluid flow and the numbers of transmigrating leukocytes reach their maximum between 6 and 12 days after the onset of clinical gingivitis.

The amount of collagen destruction increases 70% of the collagen is destroyed around the cellular infiltrate. The main fiber groups affected appear to be the circular and dentogingival fiber assemblies. Alterations in blood vessel morphologic features and vascular bed patterns have also been described.

PMNs that have left the blood vessels in response to chemo- tactic stimuli from plaque components travel to the epithelium,

cross the basement lamina, and are found in the epithelium, emerg- ing in the pocket area. PMNs are attracted to bacteria and engulf them in the process of phagocytosis . PMNs release their lysosomes in association with the ingetion of bacteria.Fibroblasts show cytotoxic alterations, with a decreased capacity for collagen.

Meanwhile, on the opposite side of molecular events, collagen degradation is related to matrix metalloproteins (MMPs). Different MMPs are responsible for extracellular matrix remodeling within 7 days of inflammation, which is directly related to MMP-2 and MMP-9 production and activation.

STAGE III GINGIVITIS: THE ESTABLISHED LESION

Over time, the established lesion evolves, characterized by a predominance of plasma cells and B lymphocytes and probably in conjuncation with the creation of a small gingival pocket lined with a pocket epithelium.The B cells found in the established lesion are pre- dominantly of the immunoglobulin G1 (IgG1) and G3 (IgG3) subclasses.

In chronic gingivitis, which occurs 2 to 3 weeks after the beginning of plaque accumulation, the blood vessels become engorged and congested, venous return is impaired, and the blood flow becomes sluggish .The result is localized gingival anoxemia, which superimposes a somewhat bluish hue on the reddenedgingiva.18 Extravasation of erythrocytes into the connective tissue and breakdown of hemoglobin into its component pigments can also deepen the color of the chronically inflamed gingiva. The established lesion can be described as moderately to severely inflamed gingiva.

An inverse relationship appears to exist between the number of intact collagen bundles and the number of inflammatory cells.Collagenolytic activity is increased in inflamed gingival tissue17 by the enzyme collagenase. Collagenase is normally present in gingival tissues5 and is produced by some oral bacteria and by PMNs.

Enzyme histochemistry studies have shown that chronically inflamed gingivae have elevated levels of acid and alkaline phos- phatase, β-glucuronidase, β-glucosidase, β-galactosidase, esterases, aminopeptidase, and cytochrome oxidase. Neutral mucopolysaccharide levels are decreased, presumably as a result of degradation of the ground substance.

Established lesions of two types appear to exist; some remain stable and do not progress for months or years and others seem to become more active and to convert to progressively destructive lesions. Also, the established lesions appear to be reversible in that the sequence of events occurring in the tissues as a result of successful periodontal therapy seems to be essentially the reverse of the sequence of events observed as gingivitis develops. As the flora reverts from that characteristically associated with destructive lesions to that associated with periodontal health, the percentage of plasma cells decreases greatly, and the lymphocyte population increases proportionately.

STAGE IV GINGIVITIS: THE ADVANCED LESION

Extension of the lesion into alveolar bone characterizes a fourth stage known as the advanced lesion or phase of periodontal break- down.

Gingivitis will progress to periodontitis only in individuals who are susceptible. Patients who had sites with consistent bleeding had 70% more attachment loss than at sites that were not inflamed consistently (GI = 0). Teeth with noninflamed sites consistently had a 50-year survival rate of 99.5%, whereas teeth with consistently inflamed gingiva had a 63.4% survival rate over 50 years. Based on this longitudinal study on the natural history of periodontitis in a well-maintained male population, per- sistent gingivitis represents a risk factor for periodontal attachment loss and for tooth loss.

Reference- Caranza textbook of periodontology 11th edition