STUDY - Technical - New Dacian's Medicine
Oral
manifestations of diseases
Translation Draft
A full examination of the oral cavity, including soft oral and pharyngeal tissues, as well as teeth, is an important part of the physical examination. Common oral diseases are due to infection with bacteria, grease swells or viruses. The complex development of orofacial structures leads to the close interposition of a large variety of tissues, most of which are prone to developmental abnormalities, growth disorders and neoplasia.
I'm going to start with tooth damage, specifically tooth decay, pulp and periapical disorders and complications.
Tooth decay is a destructive disease of hard dental tissues due to infection with Streptococcus mutans and other bacteria. One of the most widespread diseases of man in the past, caries have exhibited important changes in recent years.
Thus, less than half of people aged 17 years or younger currently have carious injuries, although in many segments of the population and in developing countries there has been no such decrease. Much of this effect is due to artificial fluoridation of drinking water up to the level of 1 in a million (where applicable), with additional effects due to fluoride-containing toothpastes and topical fluoride administration.
On the other hand, tooth retention and an ageing population have led to an increase in the number of root caries. Increasing the number of patients who survive with the consequences of anticancer treatment and other special categories of population (diabetics and those with xerostomy due to Sjogren's syndrome or medicines), may experience severe cavities if adequate topical fluoride prophylaxis is not used.
Treatment of caries involves removal of hard and infected tissues, sealing exposed dentin and restoration of lost dental structure with silver, composite, gold or porcelain amalgam. If the lesion progresses, infection of the dental pulp that causes acute pulpitis may occur. The tooth can become sensitive to hot or cold, after which severe, continuous, pulsating pain occurs. At this stage, the pulp lesion is irreversible and treatment of the root canal becomes necessary.
The contents of the pulp chamber and root canals are removed, after which the thorough cleaning, antisepsis and filling with an inert material follows. Alternatively, tooth extraction may be indicated. If pulpitis is not treated effectively, the infection can spread beyond the apex of the tooth into the periodontal ligament.
If the infection causes acute inflammation, pain occurs when chewing or percussion and a periapical abscess may form, while chronic inflammation can produce a periapical granuloma in the structure of the alveolar bone. It can cause mild pain and tenderness or it can be asymptomatic. The proliferation of epithelial cell debris can turn granuloma into a periapical cyst. Both granuloma and cyst do not produce periapical radiotransparency unless they form as a complication of one of the two lesions. The purpour in the periapical abscess can diffuse through the alveolar bone into the soft tissues, producing cellulite and bacteremia, or it can drain into the oral cavity (hair or gigival abscess), the maxillary sinus or through the skin of the face or submandibular region. A severe form of cellulitis, angina Ludwig, originates in an infected mandibular molar, affects the submandibular space and extends to the entire oral floor, with tongue lifting, dysphagia and dyspnoea. Glotic edema may occur, requiring emergency tracheotomy.
Let's now proceed to the presentation of the effect of systemic factors on the teeth. Systemic factors, occurring in utero or in childhood, during the stages of crown formation, can influence the development and structure of the teeth.
Hypoplasia of primary and/ or permanent tooth, manifested by changes ranging from white spots to major defects in crown surface structure, may also be caused by disorders of calcium and phosphorus metabolism, such as those found in vitamin D-resistant rickets, hypoparathyroidism, gastroenteritis and celiac disease. Premature birth or episodes of high fever can also cause malt hypoplasia.
Tetracycline administered in the second half of pregnancy, during the infant period and in childhood up to the age of 8 years, produces both a permanent change in the color of the teeth and the hypoplasia of the tooth. Daily ingestion of more than 1.5 mg fluorides can lead to changes in the color of the malt (marble). Prenatal factors seem to influence the size of the crown.
Larger teeth are associated with maternal diabetes, maternal hypothyroidism and large waists at birth. Tooth size is reduced in Down syndrome. Premature loss of decidual teeth is often the first symptom in juvenile hypophosphataseemia.
Systemic diseases can cause pain that simulates a pulp disorder. Jaw sinusitis is commonly manifested with pain in the jaw teeth, including sensitivity to thermal changes and percussion. Cardiac pathology with angina can produce irradiated pain in the mandible, probably through the vagus nerve.
I will now address the diseases of the parodont. In adults, chronic destructive periodontal diseases become responsible for the loss of more teeth than caries, especially in the elderly. However, the prevalence and incidence of parodontial diseases also appear to be decreasing. The most common form of periodontal disease begins with an inflammation of the edge of the gum (gingivitis), which is painless, although the gums may bleed when brushing.
The disease spreads with interest to the periodontal ligament and the alveolar bone. As the latter is slowly resorbed, a loss of attachment of the periodontal ligament between the tooth and bone occurs. Soft tissue separates from the surface of the tooth, causing the formation of a "pocket" of bleeding on examination and during chewing.
Acute inflammation can be overadded to this chronic process, with the production of pus and the formation of a periodontal abscess. Finally, excessive bone loss, tooth mobility and the formation of recurrent abscesses lead to exfoliation or may require tooth extraction. Gingivitis and periodontitis can be infections associated with the accumulation of bacterial plaque, which can be mineralized (tartar) and which can be prevented by appropriate oral hygiene measures, which requires brushing of teeth, the use of dental floss, antibacterial mouthwashes and removal of fixed food scraps.
Improperly manufactured or damaged dental work can contribute through excess or inadequate edges, while the role of occlusive trauma is unclear. Treatment concerns causative microflora and consists in the removal of plaque and tartar, the debridement of the inner surface of the "pockets" and the infected superficial cement and the elimination of other determinants. Periodontal disease appears to be a group of conditions, including adult periodontitis, associated with Porphyromonas gingivalis, Prevotella intermedia and other gram-negative microorganisms. Localized juvenile periodontitis (PJL) causes rapid periodontal "pockets" and bone loss, being associated with Actinobacillus actinomycetcomitans, Capnocytophaga, Eikenella corrodens and other anaerobics. Acute necrotizing ulcerative gingivitis (GUNA) involves acute inflammation of the gums, with necrosis, tissue loss, pain, bleeding and halitosis and is associated with P. intermedia and spirochetes.
GUNA and an aggressive and rapid form of periodontitis (necrotizing ulcerative periodontitis) are found in association with HIV infection. Some of these cases progress to a destructive lesion, similar to gangrene, soft oral tissues and bone (necrotizing stomatitis), similar to the noma found in populations with severe malnutrition. Treatment involves local antibacterial measures, debridement and, in severe cases, effective antibiotics against gram-negative anaerobics, administered systemically.
Host factors may be involved in the pathogenesis of periodontal disease and in other populations. Thus, the PJL identifies familial defects of neutrophil chemotaxia and these may predispose to tissue destruction caused by the toxins of the microorganism A. actinomyetemcomitans, including leukotoxin, colagenesis, endotoxin and a factor that further inhibits neutrophil chemotaxia. Patients with IgA and agamaglobulinemia deficiency probably have fewer periodontal diseases than healthy individuals, while in Down syndrome and diabetes mellitus a serious periodontal disease may occur.
During pregnancy, severe gingivitis and the formation of localized pyogen granulomas may occur. Certain medicines, in particular the phenytoin anticonvulsant and the calcium channel blocker antianginos drug, nifedipine, produce fibrous hyperplasia of the gum, which can cover the teeth, interfere with the feeding process and be unsightly.
Similar clinical manifestations may be due to idiopathic familial gingival fibromatosis. In both situations surgical treatment is used, although a change in medication may be appropriate for the drug-induced form. Periapical and periodontal bacterial infections can cause transient bacteremia after dental extractions and even after routine dental prophylaxis. These may cause bacterial endocarditis in patients with a history of acute joint rheumatism, other valvular diseases, valvular grafts or cardiac or joint prostheses. Antibiotic protection is appropriate in such cases.
Tomorrow I will continue with oral mucosa disorders...
A full examination of the oral cavity, including soft oral and pharyngeal tissues, as well as teeth, is an important part of the physical examination. Common oral diseases are due to infection with bacteria, grease swells or viruses. The complex development of orofacial structures leads to the close interposition of a large variety of tissues, most of which are prone to developmental abnormalities, growth disorders and neoplasia.
I'm going to start with tooth damage, specifically tooth decay, pulp and periapical disorders and complications.
Tooth decay is a destructive disease of hard dental tissues due to infection with Streptococcus mutans and other bacteria. One of the most widespread diseases of man in the past, caries have exhibited important changes in recent years.
Thus, less than half of people aged 17 years or younger currently have carious injuries, although in many segments of the population and in developing countries there has been no such decrease. Much of this effect is due to artificial fluoridation of drinking water up to the level of 1 in a million (where applicable), with additional effects due to fluoride-containing toothpastes and topical fluoride administration.
On the other hand, tooth retention and an ageing population have led to an increase in the number of root caries. Increasing the number of patients who survive with the consequences of anticancer treatment and other special categories of population (diabetics and those with xerostomy due to Sjogren's syndrome or medicines), may experience severe cavities if adequate topical fluoride prophylaxis is not used.
Treatment of caries involves removal of hard and infected tissues, sealing exposed dentin and restoration of lost dental structure with silver, composite, gold or porcelain amalgam. If the lesion progresses, infection of the dental pulp that causes acute pulpitis may occur. The tooth can become sensitive to hot or cold, after which severe, continuous, pulsating pain occurs. At this stage, the pulp lesion is irreversible and treatment of the root canal becomes necessary.
The contents of the pulp chamber and root canals are removed, after which the thorough cleaning, antisepsis and filling with an inert material follows. Alternatively, tooth extraction may be indicated. If pulpitis is not treated effectively, the infection can spread beyond the apex of the tooth into the periodontal ligament.
If the infection causes acute inflammation, pain occurs when chewing or percussion and a periapical abscess may form, while chronic inflammation can produce a periapical granuloma in the structure of the alveolar bone. It can cause mild pain and tenderness or it can be asymptomatic. The proliferation of epithelial cell debris can turn granuloma into a periapical cyst. Both granuloma and cyst do not produce periapical radiotransparency unless they form as a complication of one of the two lesions. The purpour in the periapical abscess can diffuse through the alveolar bone into the soft tissues, producing cellulite and bacteremia, or it can drain into the oral cavity (hair or gigival abscess), the maxillary sinus or through the skin of the face or submandibular region. A severe form of cellulitis, angina Ludwig, originates in an infected mandibular molar, affects the submandibular space and extends to the entire oral floor, with tongue lifting, dysphagia and dyspnoea. Glotic edema may occur, requiring emergency tracheotomy.
Let's now proceed to the presentation of the effect of systemic factors on the teeth. Systemic factors, occurring in utero or in childhood, during the stages of crown formation, can influence the development and structure of the teeth.
Hypoplasia of primary and/ or permanent tooth, manifested by changes ranging from white spots to major defects in crown surface structure, may also be caused by disorders of calcium and phosphorus metabolism, such as those found in vitamin D-resistant rickets, hypoparathyroidism, gastroenteritis and celiac disease. Premature birth or episodes of high fever can also cause malt hypoplasia.
Tetracycline administered in the second half of pregnancy, during the infant period and in childhood up to the age of 8 years, produces both a permanent change in the color of the teeth and the hypoplasia of the tooth. Daily ingestion of more than 1.5 mg fluorides can lead to changes in the color of the malt (marble). Prenatal factors seem to influence the size of the crown.
Larger teeth are associated with maternal diabetes, maternal hypothyroidism and large waists at birth. Tooth size is reduced in Down syndrome. Premature loss of decidual teeth is often the first symptom in juvenile hypophosphataseemia.
Systemic diseases can cause pain that simulates a pulp disorder. Jaw sinusitis is commonly manifested with pain in the jaw teeth, including sensitivity to thermal changes and percussion. Cardiac pathology with angina can produce irradiated pain in the mandible, probably through the vagus nerve.
I will now address the diseases of the parodont. In adults, chronic destructive periodontal diseases become responsible for the loss of more teeth than caries, especially in the elderly. However, the prevalence and incidence of parodontial diseases also appear to be decreasing. The most common form of periodontal disease begins with an inflammation of the edge of the gum (gingivitis), which is painless, although the gums may bleed when brushing.
The disease spreads with interest to the periodontal ligament and the alveolar bone. As the latter is slowly resorbed, a loss of attachment of the periodontal ligament between the tooth and bone occurs. Soft tissue separates from the surface of the tooth, causing the formation of a "pocket" of bleeding on examination and during chewing.
Acute inflammation can be overadded to this chronic process, with the production of pus and the formation of a periodontal abscess. Finally, excessive bone loss, tooth mobility and the formation of recurrent abscesses lead to exfoliation or may require tooth extraction. Gingivitis and periodontitis can be infections associated with the accumulation of bacterial plaque, which can be mineralized (tartar) and which can be prevented by appropriate oral hygiene measures, which requires brushing of teeth, the use of dental floss, antibacterial mouthwashes and removal of fixed food scraps.
Improperly manufactured or damaged dental work can contribute through excess or inadequate edges, while the role of occlusive trauma is unclear. Treatment concerns causative microflora and consists in the removal of plaque and tartar, the debridement of the inner surface of the "pockets" and the infected superficial cement and the elimination of other determinants. Periodontal disease appears to be a group of conditions, including adult periodontitis, associated with Porphyromonas gingivalis, Prevotella intermedia and other gram-negative microorganisms. Localized juvenile periodontitis (PJL) causes rapid periodontal "pockets" and bone loss, being associated with Actinobacillus actinomycetcomitans, Capnocytophaga, Eikenella corrodens and other anaerobics. Acute necrotizing ulcerative gingivitis (GUNA) involves acute inflammation of the gums, with necrosis, tissue loss, pain, bleeding and halitosis and is associated with P. intermedia and spirochetes.
GUNA and an aggressive and rapid form of periodontitis (necrotizing ulcerative periodontitis) are found in association with HIV infection. Some of these cases progress to a destructive lesion, similar to gangrene, soft oral tissues and bone (necrotizing stomatitis), similar to the noma found in populations with severe malnutrition. Treatment involves local antibacterial measures, debridement and, in severe cases, effective antibiotics against gram-negative anaerobics, administered systemically.
Host factors may be involved in the pathogenesis of periodontal disease and in other populations. Thus, the PJL identifies familial defects of neutrophil chemotaxia and these may predispose to tissue destruction caused by the toxins of the microorganism A. actinomyetemcomitans, including leukotoxin, colagenesis, endotoxin and a factor that further inhibits neutrophil chemotaxia. Patients with IgA and agamaglobulinemia deficiency probably have fewer periodontal diseases than healthy individuals, while in Down syndrome and diabetes mellitus a serious periodontal disease may occur.
During pregnancy, severe gingivitis and the formation of localized pyogen granulomas may occur. Certain medicines, in particular the phenytoin anticonvulsant and the calcium channel blocker antianginos drug, nifedipine, produce fibrous hyperplasia of the gum, which can cover the teeth, interfere with the feeding process and be unsightly.
Similar clinical manifestations may be due to idiopathic familial gingival fibromatosis. In both situations surgical treatment is used, although a change in medication may be appropriate for the drug-induced form. Periapical and periodontal bacterial infections can cause transient bacteremia after dental extractions and even after routine dental prophylaxis. These may cause bacterial endocarditis in patients with a history of acute joint rheumatism, other valvular diseases, valvular grafts or cardiac or joint prostheses. Antibiotic protection is appropriate in such cases.
Tomorrow I will continue with oral mucosa disorders...
Have a good day!
Dorin, Merticaru