Periodontal traumatism
Excessive occlusal forces result in typical changes in the periodontal ligament and also bone. If these abnormal occlusal forces are chronic and repeated over a long period of time, the periodontal ligament gradually becomes denser and the periodontal space widens. The alveolar bone becomes denser also and the teeth will show obvious linear patterns, with definite facets on the crowns of teeth.
An acute traumatic force sufficient to produce traumatic injury to the periodontium also results in rather specific changes in the tooth attachment apparatus. For example a force which tips a tooth sharply to the buccal side results in a crushing of the periodontal ligament fibres and perhaps of the alveolar crest bone. The blood vessels in the involved area become thrombosed, and edema and extravasations of blood occurs. On the opposite side of the tooth there is often a tear of the periodontal ligament and sometimes cementum or bone is torn loose.
Since the tooth rotates around a fulcrum point slightly apical to the mid root, the same changes may occur near the apex on the opposite side. These changes results in tenderness of the tooth for a few days but if the forces are not grossly excessive, eventually the damaged alveolar crest bone will be resorbed, new periodontal fibres, cementum and bone will be elaborated and after a few weeks the tissues will return to normal with the periodontal ligament space wider or the tooth reoriented in a new position. When excessive forces occur in different and alternating directions, as may happen in cases of cusp interference, destruction of the supporting bone may occur around the entire periphery of the root, resulting in widening of the periodontal ligament space. This in turn, by interfering with mastication, favours collection of debris on teeth and predisposes to further periodontal disease.
PERIODONTITIS
Other names- perodontoclasia, pyorrhea, pyorrhea alveolaris, schmutz pyorrhea
The most common form of periodontal disease is that which is associated with local irritation. This begins as a marginal gingivitis which usually progresses, if untreated or treated improperly, to destructive chronic periodontitis. This marginal periodontitis is most common in adult but occasionally seen in children especially when there is poor oral hygiene or in certain cases of malocclusion. In adult chronic periodontitis account for more than 90% of periodontal diseases and is responsible for greater tooth mortality than dental caries.
Treatment of the condition depends on the removal of etiologic factors, both local & systemic, maintenance of good oral hygiene and establishment of a stable, harmonious articulation free from traumatic interference.
ETIOLOGY- gingivitis may precede and develop into the more severe periodontitis which involves not only the gingiva, but also alveolar bone, cementum and periodontal ligament. Etiologic factors in general are the same as for gingivitis but are usually more severe or of longer donation. Local factors, microbial plaque, calculus, food impaction and irritating margins of fillings appear to be most important in the development of the common form of periodontal disease. The micro- flora in advanced periodontal disease is characterized by the presence of large numbers of asacharolytic micro- organs, including fuso bacterium nucleatum, bacteroides mellaninogenicus, eikenella corrodens bacteroides corrodens bacteroides capillosus. Slots (1977) found that these organisms constituted up to 75percent of the isolates from periodontitis pockets.
Incidence- This is difficult to determine. According to some studies, the condition rarely occur before 18yaers of age but after this age incidence increases rapidly such that by 45 years of age all subjects show evidence of the disease. No abnormal mobility of tooth before 25 years of age but mobility increases sharply from 25% at 35 to 39- 49% at ages 40-48 with a steady increase to 79% at 60years.
Clinical feature-This condition usually begins as a simple marginal gingivitis as a reaction to plaque or calculus. An early and perhaps the first finding is a tiny ulceration of the crevicular epithelium. Unless the irritants are removed, with the passage of time, more plaque and calculus are deposited and the marginal gingivitis becomes more severe. The gingival becomes more inflamed and swollen and with irritations, the crevicular epithelium suffers more frequent ulceration. It proliferates as a result of the inflammation, so that at this stage there is a tendency for the epithelial attachment to extend or migrate apically on the toot. As it does so, it is easily detached at its coronal portion. Through this process and because of the increased swelling of the marginal gingival, the gingival crevice gradually becomes deeper and is classified as an early periodontal pocket. Clinically, calculus can be detected. Subgingival calculus is seen beneath the free gingival margin when it is blown back from the tooth by compressed air.
Bleeding from the interdental papillae can be easily elicited. An unpleasant, almost foul type of halitoses may also be present. As the periodontitis become more severe, the teeth become more mobile and give off a rather dull sound when tapped with a metal instrument. Suppurative materials and other debris occasionally may be expressed from the pathologic pocket adjacent to a tooth by a slight pressure on the gingival. The normal festoon of the gingival is lost and the gingivae appear boggy because of hyperemia and edema, no stippling is noted and the gingival tissues are smooth shiny and perhaps redder or bluer than normal. Patients may complain of bad taste, bleeding gums and hypersensitivity of the necks of the teeth due to exposure of cementum as the soft tissues recede. In other words, the patient has a severe chronic gingivitis and an involvement of the deeper portions of the periodontium- stage of severe periodontitis.
Gingival recession is a common phenomenon, particularly in later years in life. In such cases the gingival tissues recede towards the apex, exposing cementum, sometimes to an alarming degree. Since cementum is softer than enamed it is often worn away by a tooth brush and an abrasive dentrifice. Gingival recession can occur more rapidly if there has been rapid alveolar bone loss, due to any cause since gingival tissue in health will maintain uniform relation with alveolar bone crest. Gingival recession often begins as a thin break in the free gingival adjacent to the centre of a tooth. This is called a stillmans cleft. Abnormal frequency and directions of tooth brushing, occlusal forces or a high muscle attachment will sometimes lead to gingival recession. Gingival recession is preceded by alveolar bone loss, but bone loss is not necessarily accompanied by an equal amount of recession.
histologic feature- In marginal gingivitis which is just beginning to undergo transition into early periodontitis, the enlarged free marginal gingival is densely infiltrated with lymphocytes and plasma cells and the apical border of the inflammeed area approaches the crest of the alveolar bone and the crestal fibres of the periodontal ligament. One of the early microscopic signs of the encroachment of the inflammatory process on the periodontium is the appearance of giant cells, osteoclasts on the surfaces of the bone crest. They soon appear to lie in the little bays of bone resorption known as howships lacunae. The underlying tissues of the periodontium show no changes at this stage. The pathologic process involves alveolar bone prior to involvement of the periodontal ligament.
The next stage of the process of the disease is a continuation of the factors just described –
1- More plaque is deposited in an apical direction on the tooth.
2- More irritation of the free gingival occurs.
3- The epithelial attachment proliferates apically down in to the cementium of the tooth and shows more ulceration.
4- The alveolar crest of the bone is resorbed further apically
5- Principal periodontal ligament fibres become disorganized and detached from the tooth.
6- A periodontal pocket exists between the free gingiva and the tooth, to the depths of from 2mm down, until finally the apex of the tooth is approached. The deep pocket that then exists between the calculus & plaque covered tooth surface and the epithelial lining of the gingival tissues forms a protective trap for multiplying micro organisms and for leukocytic cellular exudates from the inflamed soft tissues of the pocket wall. The vicious cycle of irritants collection, inflammation and detachment continues, along with periodontal bone resorption in an apical direction.
a. Classification of pockets
In a normal healthy periodontium, the gingival tissues fit snugly around the teeth, and the gingival crevice approximate zero. In the presence of inflammation however, the gingival tissues increases in bulk, causing an increase in the depth of the pocket around the teeth. If the pathologic changes are limited to the gingival this is called a gingival (or pseudo) pocket. If however the base of the pocket has invaded further into the periodontium it is called a periodontal pocket. The base of the periodontal pocket is on the tooth root, and the epithelial attachment is on the cementum. Although periodontal diseases usually progresses apically and advances at the expense of the horizontal loss of the crest of the alveolar bone, sometimes the depth of the pocket extends apical to the crest of the alveolar bone. Such a pocket,which has bone on its lateral wall is called an infra- bony pockets and is the exception rather than the rule, since usually the bottom of the pathologic pockets is level with or coronal to the alveolar crest of bone(supra- bony pocket). The infrabony pockets may result from food impaction and is frequently found along the tooth which has shifted considerably out of its usual position or has been subjected to severe occlusal trauma. Infra-bony pockets are classified according to their shape (narrow or broad) and the numbers of bony walls.
Gingival Hyperplasia - enlargement of gingival.
It may be localized to one papilla or may involve several or all of the gingival papillae throughout the mouth. Enlargement is more prominent in labial or buccal surfaces. Occasionally may occur on lingual surface. It does not involve vestibular mucosa.
An increase in the bulk of the tissue may be due to hypertrophy I e an increase in the size of a structure due to an increase in the size of the individual cells involved or due to hyperplasia I e an increase in the number of cellular elements. Gingival hyperplasia is a general term for the gross increase in size of gingival tissues which may result from a number of different conditions.Do not confuse gingival enlargement with bone exostoses (overgrowth of bone)
Classification of hyperplasia
1. Inflammatory gingival hyperplasia
2. Non- inflammatory fibrous hyperplasia.
3. Combination of inflammatory and non inflammatory fibrous hyperplasia.
In inflammatory hyperplasia, the enlarged gingivae are soft, edematous, hyperemic or cyanotic and sensitive to touch. Bleed easily & present a glossy non-stippled surface.
In fibrous gingival hyperplasia- enlarged tissue is firm, dense, resilient, normal in color or slightly paler than normal sometimes well stippled, insensitive and not easily traumatized. Frequently there is a combination of the two types of enlargement. These enlargements results because of local irritants such as poor oral hygiene, accumulation of dental calculus or mouth breathing.
Inflammatory gingival hyperplasia
This usually results from prolonged chronic inflammation of the gingival tissues. Clinical examination will reveal the nature of the local irritation that causes the hyperplasia but the histologic picture is usually non specific showing merely inflammation of the gingival.
Inflammatory hyperplasia associated with vitamin C deficiency, present as a spongy bleeding gum of scurvy (vit c def). Clinical scurvy is now rare but occasional cases are seen. The gingivae become tender, swollen and edematous. Bleed upon the slightest provocation. Gingival sulci are often filled with partially clotted blood and the crests of the interdental papillae are red or purple. Hemorrhages following slight trauma to other parts of the body are also noted. Treatment – improvement of oral hygiene and administration of vitamin c.
Inflammatory hyperplasia associated with leukemia
Gingival hyperplasia is often an early finding in acute monocytic, lymphocytic or myelocytic leukaenias. Gingival tissues are enlarged and are soft, edematous, easily compressed and tender. No sign of stippling. Color of gingiva is sometimes bluish red and the surface is glossy. Gingival is usually inflamed due to local infection and at times ANUG may develop.
Inflammatory hyperplasia due to endocrine imbalance
The gingival hyperplasia often occurs at puberty, particularly in females (girls). During, pregnancy one also notices tendency for gingival hyperplasia of the inflammatory type. This proliferation may be due to disturbed nutrition, poor oral hygiene or actually some systemic predisposition towards proliferation. Pregnancy gingivitis is often associated with isolated gingival proliferation, sometimes so severe that it is referred to as pregnancy tumour which is basically pyogenic granuloma. . Histology shows increased vascularity, multiplication of fibroblasts, edema and infiltration of leukocytes into the gingiva. Diagnosis of the etiologic factors cannot be made by microscopic study.
Inflammatory hyperplasis associated with regional enteritis
(crohn’s disease)- a slowly progressive disease of unknown etiology occurring in persons of all ages and both sex. It is characterized by granulomatous,, superficial ulceration of the intestinal tract with frequent fistulae developing onto body surfaces or viscera or between intestinal loops. This disease has been reported as having oral manifestation or oral extensions. The most commonly involved areas are the buccal mucosa where the lesions present a cobble stone apprearance; the vestibule, where linear, hyperplastic folds and ulcers are found. The lips which appear diffusely swollen and indurated; the gingival and alveolar mucosa which exhibit a granular erythematous swelling and the palate where multiple ulcers occur. Oral lesions may show periods of quiescence alternating with exacerbations of the process. Histology finding of oral lesions are those of a chronic granulomatous disease reminiscent of sarcoid.
Fibrous hyperplasia of gingiva
Histology shows that the enlargement is due primarily to an increase in the bulk of the mature fibrous connective tissues. Occasionally inflammatory changes are superimposed on the fibrous hyperplasia.
Chronic low grade irritation of a gingival tissue can cause localized hyperplasia of fibrous tissues. The treatment is to remove the local irritation. If the fibrous hyperplasia is too extensive, surgical excision is desirable. The fibrous hyperplasia may gradually progress although it is usually self limiting.
Idiopathic fibrous hyperplasia
Fibromatosis gingivae; elephantiasis gingivae, and congenital macro gingivae. The gingival are so diffusely enlarged that the teeth are covered or if the enlargement is present before tooth erupt the dense fibrous tissues may interfere with or prevent eruption. Etiology is unknown and it is probably genetic in some instances.
This hyperplasia may be noted at an early age and in a few cases even at birth. Teeth do not errupt normally because of the dense fibrous tissues.
Histology- sections show a moderate hyperplasia of the epithelium with mild hyperkeratosis and production of long rete pegs. The underlying stroma is made up of almost entirely of dense bundles of mature fibrous tissues with few young fibroblast present. Occasionally some chronic inflammation caused by local irritation may also be present. Surgical removal of the excess fibrous tissues is the only treatment of value. Recurrence may follow.
Fibrous hyperplasia caused by dilantin sodium
This fibrous hyperplasia occur as a result of the anti convulsant drug- diphenyl hydatoin (dilantin sodium) the drug is very effective in controlling epileptic seizures, but in some cases does have the side effect of causing fibrous hyperplasia of the gingival. The gingival hyperplasia may arise shortly after institution of dilantin sodium therapy. It begins with the painless enlargement of one or two interdental papillae which present an increased stippling and ultimately a roughened pebbled surface with lobulations.
The gingival tissues are dense, resilient and insensitive. They show little or no tendency to bleed. The bulk of the enlargement is due primarily to proliferation of the fibrous connective tissues with numerous fibroblasts. There may be a superimposed chronic inflammation. The enlargement generally presents no difficulties, although it is esthetically objectionable. It may be so severe as to interfere with function and for this reason it may be surgically excised. Unfortunately recurrence is common. It has been found that careful oral hygiene will result in slower development of the hyperplasia and slower recurrence after surgical excision. Some regression of the hyperplasia may result if the use of the drug is discontinued
Excessive occlusal forces result in typical changes in the periodontal ligament and also bone. If these abnormal occlusal forces are chronic and repeated over a long period of time, the periodontal ligament gradually becomes denser and the periodontal space widens. The alveolar bone becomes denser also and the teeth will show obvious linear patterns, with definite facets on the crowns of teeth.
An acute traumatic force sufficient to produce traumatic injury to the periodontium also results in rather specific changes in the tooth attachment apparatus. For example a force which tips a tooth sharply to the buccal side results in a crushing of the periodontal ligament fibres and perhaps of the alveolar crest bone. The blood vessels in the involved area become thrombosed, and edema and extravasations of blood occurs. On the opposite side of the tooth there is often a tear of the periodontal ligament and sometimes cementum or bone is torn loose.
Since the tooth rotates around a fulcrum point slightly apical to the mid root, the same changes may occur near the apex on the opposite side. These changes results in tenderness of the tooth for a few days but if the forces are not grossly excessive, eventually the damaged alveolar crest bone will be resorbed, new periodontal fibres, cementum and bone will be elaborated and after a few weeks the tissues will return to normal with the periodontal ligament space wider or the tooth reoriented in a new position. When excessive forces occur in different and alternating directions, as may happen in cases of cusp interference, destruction of the supporting bone may occur around the entire periphery of the root, resulting in widening of the periodontal ligament space. This in turn, by interfering with mastication, favours collection of debris on teeth and predisposes to further periodontal disease.
PERIODONTITIS
Other names- perodontoclasia, pyorrhea, pyorrhea alveolaris, schmutz pyorrhea
The most common form of periodontal disease is that which is associated with local irritation. This begins as a marginal gingivitis which usually progresses, if untreated or treated improperly, to destructive chronic periodontitis. This marginal periodontitis is most common in adult but occasionally seen in children especially when there is poor oral hygiene or in certain cases of malocclusion. In adult chronic periodontitis account for more than 90% of periodontal diseases and is responsible for greater tooth mortality than dental caries.
Treatment of the condition depends on the removal of etiologic factors, both local & systemic, maintenance of good oral hygiene and establishment of a stable, harmonious articulation free from traumatic interference.
ETIOLOGY- gingivitis may precede and develop into the more severe periodontitis which involves not only the gingiva, but also alveolar bone, cementum and periodontal ligament. Etiologic factors in general are the same as for gingivitis but are usually more severe or of longer donation. Local factors, microbial plaque, calculus, food impaction and irritating margins of fillings appear to be most important in the development of the common form of periodontal disease. The micro- flora in advanced periodontal disease is characterized by the presence of large numbers of asacharolytic micro- organs, including fuso bacterium nucleatum, bacteroides mellaninogenicus, eikenella corrodens bacteroides corrodens bacteroides capillosus. Slots (1977) found that these organisms constituted up to 75percent of the isolates from periodontitis pockets.
Incidence- This is difficult to determine. According to some studies, the condition rarely occur before 18yaers of age but after this age incidence increases rapidly such that by 45 years of age all subjects show evidence of the disease. No abnormal mobility of tooth before 25 years of age but mobility increases sharply from 25% at 35 to 39- 49% at ages 40-48 with a steady increase to 79% at 60years.
Clinical feature-This condition usually begins as a simple marginal gingivitis as a reaction to plaque or calculus. An early and perhaps the first finding is a tiny ulceration of the crevicular epithelium. Unless the irritants are removed, with the passage of time, more plaque and calculus are deposited and the marginal gingivitis becomes more severe. The gingival becomes more inflamed and swollen and with irritations, the crevicular epithelium suffers more frequent ulceration. It proliferates as a result of the inflammation, so that at this stage there is a tendency for the epithelial attachment to extend or migrate apically on the toot. As it does so, it is easily detached at its coronal portion. Through this process and because of the increased swelling of the marginal gingival, the gingival crevice gradually becomes deeper and is classified as an early periodontal pocket. Clinically, calculus can be detected. Subgingival calculus is seen beneath the free gingival margin when it is blown back from the tooth by compressed air.
Bleeding from the interdental papillae can be easily elicited. An unpleasant, almost foul type of halitoses may also be present. As the periodontitis become more severe, the teeth become more mobile and give off a rather dull sound when tapped with a metal instrument. Suppurative materials and other debris occasionally may be expressed from the pathologic pocket adjacent to a tooth by a slight pressure on the gingival. The normal festoon of the gingival is lost and the gingivae appear boggy because of hyperemia and edema, no stippling is noted and the gingival tissues are smooth shiny and perhaps redder or bluer than normal. Patients may complain of bad taste, bleeding gums and hypersensitivity of the necks of the teeth due to exposure of cementum as the soft tissues recede. In other words, the patient has a severe chronic gingivitis and an involvement of the deeper portions of the periodontium- stage of severe periodontitis.
Gingival recession is a common phenomenon, particularly in later years in life. In such cases the gingival tissues recede towards the apex, exposing cementum, sometimes to an alarming degree. Since cementum is softer than enamed it is often worn away by a tooth brush and an abrasive dentrifice. Gingival recession can occur more rapidly if there has been rapid alveolar bone loss, due to any cause since gingival tissue in health will maintain uniform relation with alveolar bone crest. Gingival recession often begins as a thin break in the free gingival adjacent to the centre of a tooth. This is called a stillmans cleft. Abnormal frequency and directions of tooth brushing, occlusal forces or a high muscle attachment will sometimes lead to gingival recession. Gingival recession is preceded by alveolar bone loss, but bone loss is not necessarily accompanied by an equal amount of recession.
histologic feature- In marginal gingivitis which is just beginning to undergo transition into early periodontitis, the enlarged free marginal gingival is densely infiltrated with lymphocytes and plasma cells and the apical border of the inflammeed area approaches the crest of the alveolar bone and the crestal fibres of the periodontal ligament. One of the early microscopic signs of the encroachment of the inflammatory process on the periodontium is the appearance of giant cells, osteoclasts on the surfaces of the bone crest. They soon appear to lie in the little bays of bone resorption known as howships lacunae. The underlying tissues of the periodontium show no changes at this stage. The pathologic process involves alveolar bone prior to involvement of the periodontal ligament.
The next stage of the process of the disease is a continuation of the factors just described –
1- More plaque is deposited in an apical direction on the tooth.
2- More irritation of the free gingival occurs.
3- The epithelial attachment proliferates apically down in to the cementium of the tooth and shows more ulceration.
4- The alveolar crest of the bone is resorbed further apically
5- Principal periodontal ligament fibres become disorganized and detached from the tooth.
6- A periodontal pocket exists between the free gingiva and the tooth, to the depths of from 2mm down, until finally the apex of the tooth is approached. The deep pocket that then exists between the calculus & plaque covered tooth surface and the epithelial lining of the gingival tissues forms a protective trap for multiplying micro organisms and for leukocytic cellular exudates from the inflamed soft tissues of the pocket wall. The vicious cycle of irritants collection, inflammation and detachment continues, along with periodontal bone resorption in an apical direction.
a. Classification of pockets
In a normal healthy periodontium, the gingival tissues fit snugly around the teeth, and the gingival crevice approximate zero. In the presence of inflammation however, the gingival tissues increases in bulk, causing an increase in the depth of the pocket around the teeth. If the pathologic changes are limited to the gingival this is called a gingival (or pseudo) pocket. If however the base of the pocket has invaded further into the periodontium it is called a periodontal pocket. The base of the periodontal pocket is on the tooth root, and the epithelial attachment is on the cementum. Although periodontal diseases usually progresses apically and advances at the expense of the horizontal loss of the crest of the alveolar bone, sometimes the depth of the pocket extends apical to the crest of the alveolar bone. Such a pocket,which has bone on its lateral wall is called an infra- bony pockets and is the exception rather than the rule, since usually the bottom of the pathologic pockets is level with or coronal to the alveolar crest of bone(supra- bony pocket). The infrabony pockets may result from food impaction and is frequently found along the tooth which has shifted considerably out of its usual position or has been subjected to severe occlusal trauma. Infra-bony pockets are classified according to their shape (narrow or broad) and the numbers of bony walls.
Gingival Hyperplasia - enlargement of gingival.
It may be localized to one papilla or may involve several or all of the gingival papillae throughout the mouth. Enlargement is more prominent in labial or buccal surfaces. Occasionally may occur on lingual surface. It does not involve vestibular mucosa.
An increase in the bulk of the tissue may be due to hypertrophy I e an increase in the size of a structure due to an increase in the size of the individual cells involved or due to hyperplasia I e an increase in the number of cellular elements. Gingival hyperplasia is a general term for the gross increase in size of gingival tissues which may result from a number of different conditions.Do not confuse gingival enlargement with bone exostoses (overgrowth of bone)
Classification of hyperplasia
1. Inflammatory gingival hyperplasia
2. Non- inflammatory fibrous hyperplasia.
3. Combination of inflammatory and non inflammatory fibrous hyperplasia.
In inflammatory hyperplasia, the enlarged gingivae are soft, edematous, hyperemic or cyanotic and sensitive to touch. Bleed easily & present a glossy non-stippled surface.
In fibrous gingival hyperplasia- enlarged tissue is firm, dense, resilient, normal in color or slightly paler than normal sometimes well stippled, insensitive and not easily traumatized. Frequently there is a combination of the two types of enlargement. These enlargements results because of local irritants such as poor oral hygiene, accumulation of dental calculus or mouth breathing.
Inflammatory gingival hyperplasia
This usually results from prolonged chronic inflammation of the gingival tissues. Clinical examination will reveal the nature of the local irritation that causes the hyperplasia but the histologic picture is usually non specific showing merely inflammation of the gingival.
Inflammatory hyperplasia associated with vitamin C deficiency, present as a spongy bleeding gum of scurvy (vit c def). Clinical scurvy is now rare but occasional cases are seen. The gingivae become tender, swollen and edematous. Bleed upon the slightest provocation. Gingival sulci are often filled with partially clotted blood and the crests of the interdental papillae are red or purple. Hemorrhages following slight trauma to other parts of the body are also noted. Treatment – improvement of oral hygiene and administration of vitamin c.
Inflammatory hyperplasia associated with leukemia
Gingival hyperplasia is often an early finding in acute monocytic, lymphocytic or myelocytic leukaenias. Gingival tissues are enlarged and are soft, edematous, easily compressed and tender. No sign of stippling. Color of gingiva is sometimes bluish red and the surface is glossy. Gingival is usually inflamed due to local infection and at times ANUG may develop.
Inflammatory hyperplasia due to endocrine imbalance
The gingival hyperplasia often occurs at puberty, particularly in females (girls). During, pregnancy one also notices tendency for gingival hyperplasia of the inflammatory type. This proliferation may be due to disturbed nutrition, poor oral hygiene or actually some systemic predisposition towards proliferation. Pregnancy gingivitis is often associated with isolated gingival proliferation, sometimes so severe that it is referred to as pregnancy tumour which is basically pyogenic granuloma. . Histology shows increased vascularity, multiplication of fibroblasts, edema and infiltration of leukocytes into the gingiva. Diagnosis of the etiologic factors cannot be made by microscopic study.
Inflammatory hyperplasis associated with regional enteritis
(crohn’s disease)- a slowly progressive disease of unknown etiology occurring in persons of all ages and both sex. It is characterized by granulomatous,, superficial ulceration of the intestinal tract with frequent fistulae developing onto body surfaces or viscera or between intestinal loops. This disease has been reported as having oral manifestation or oral extensions. The most commonly involved areas are the buccal mucosa where the lesions present a cobble stone apprearance; the vestibule, where linear, hyperplastic folds and ulcers are found. The lips which appear diffusely swollen and indurated; the gingival and alveolar mucosa which exhibit a granular erythematous swelling and the palate where multiple ulcers occur. Oral lesions may show periods of quiescence alternating with exacerbations of the process. Histology finding of oral lesions are those of a chronic granulomatous disease reminiscent of sarcoid.
Fibrous hyperplasia of gingiva
Histology shows that the enlargement is due primarily to an increase in the bulk of the mature fibrous connective tissues. Occasionally inflammatory changes are superimposed on the fibrous hyperplasia.
Chronic low grade irritation of a gingival tissue can cause localized hyperplasia of fibrous tissues. The treatment is to remove the local irritation. If the fibrous hyperplasia is too extensive, surgical excision is desirable. The fibrous hyperplasia may gradually progress although it is usually self limiting.
Idiopathic fibrous hyperplasia
Fibromatosis gingivae; elephantiasis gingivae, and congenital macro gingivae. The gingival are so diffusely enlarged that the teeth are covered or if the enlargement is present before tooth erupt the dense fibrous tissues may interfere with or prevent eruption. Etiology is unknown and it is probably genetic in some instances.
This hyperplasia may be noted at an early age and in a few cases even at birth. Teeth do not errupt normally because of the dense fibrous tissues.
Histology- sections show a moderate hyperplasia of the epithelium with mild hyperkeratosis and production of long rete pegs. The underlying stroma is made up of almost entirely of dense bundles of mature fibrous tissues with few young fibroblast present. Occasionally some chronic inflammation caused by local irritation may also be present. Surgical removal of the excess fibrous tissues is the only treatment of value. Recurrence may follow.
Fibrous hyperplasia caused by dilantin sodium
This fibrous hyperplasia occur as a result of the anti convulsant drug- diphenyl hydatoin (dilantin sodium) the drug is very effective in controlling epileptic seizures, but in some cases does have the side effect of causing fibrous hyperplasia of the gingival. The gingival hyperplasia may arise shortly after institution of dilantin sodium therapy. It begins with the painless enlargement of one or two interdental papillae which present an increased stippling and ultimately a roughened pebbled surface with lobulations.
The gingival tissues are dense, resilient and insensitive. They show little or no tendency to bleed. The bulk of the enlargement is due primarily to proliferation of the fibrous connective tissues with numerous fibroblasts. There may be a superimposed chronic inflammation. The enlargement generally presents no difficulties, although it is esthetically objectionable. It may be so severe as to interfere with function and for this reason it may be surgically excised. Unfortunately recurrence is common. It has been found that careful oral hygiene will result in slower development of the hyperplasia and slower recurrence after surgical excision. Some regression of the hyperplasia may result if the use of the drug is discontinued
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