The periodontium consists of components such as the gums, alveolar bone, cementum, and periodontal ligaments.
Gingivitis
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| Proper oral hygiene (tooth brushing with a toothbrush and flossing) can effectively address the disease (Image: lanelabs) |
Poor oral hygiene leads to the accumulation of plaque on the tooth surface, resulting in an inflammatory response, which may manifest locally or spread, causing redness and swelling of the gums. In severe cases, the gums may bleed spontaneously, and the mouth may have a foul odor.
The primary treatment is proper oral hygiene (brushing with a toothbrush and flossing), which can effectively resolve the issue. Gingivitis in healthy children before puberty does not tend to progress to periodontitis (inflammation of the periodontal ligaments leading to bone resorption).
If gingivitis is not adequately managed through oral hygiene, one should consider other underlying conditions (such as leukemia, diabetes, neutropenia, vitamin C deficiency, or hormonal disorders related to puberty or pregnancy, use of anticonvulsants, and immunosuppressive drugs).
Periodontitis Before Puberty
Periodontitis in prepubescent children can lead to the loss of primary teeth before they have fully developed, often associated with systemic conditions such as neutropenia, leukocyte adhesion deficiency, hypophosphatasia, Papillon-Lefèvre syndrome, and X-linked histiocytosis. However, many cases of children may not exhibit systemic conditions. Treatment includes dental cleaning by a dentist, and extraction of affected teeth or the use of antibiotics may be necessary.
Localized Juvenile Periodontitis
Localized juvenile periodontitis is clinically characterized by rapid alveolar bone loss, especially around the incisors and permanent first molars. The disease is often associated with Actinobacillus infection. Additionally, leukocytes from patients with localized juvenile periodontitis often lose their chemotactic and phagocytic functions.
If left untreated, diseased teeth will lose their periodontal ligaments and become mobile. Treatment depends on the extent of the disease progression. Children diagnosed early, when the disease first appears, typically receive treatment to clean necrotic tissue locally, combined with antibiotics and meticulous oral hygiene. In cases where the disease has already progressed with alveolar bone loss at the time of detection, comprehensive periodontal treatment may be required, possibly including autogenous bone grafting. The prognosis depends on the severity of the disease at diagnosis and adherence to the treatment regimen.
Tooth Eruption Process
The process of tooth eruption can cause discomfort in areas where primary teeth are emerging, leading to restlessness, mild fever, and increased saliva production; however, many children exhibit no discomfort during tooth eruption. Symptomatic treatment includes allowing children to chew on cold rings and administering antipyretics and analgesics. Similar symptoms may occur when the permanent first molars emerge at age six.
Gingival Hyperplasia Due to Cyclosporine or Phenytoin
The use of cyclosporine for organ transplantation or phenytoin for epilepsy, as well as some calcium channel blockers, can cause generalized gingival hyperplasia. Phenytoin and its metabolites directly stimulate fibroblasts in the gums, leading to increased collagen synthesis. Clinical studies have shown that phenytoin causes less gingival hyperplasia in patients with meticulous oral hygiene.
Gingival hyperplasia occurs in about 10-30% of patients taking phenytoin. Severe signs include (1) gingival enlargement, sometimes covering entire teeth, (2) swollen red gums, (3) secondary infections leading to abscess formation, (4) shifting of tooth positions, and (5) hindrance in the emergence of primary teeth, affecting permanent teeth. The main approach to treatment is prevention; if possible, discontinuation of the drug along with regular dental check-ups and oral hygiene care is advised. Severe cases of gingival hyperplasia may require surgical gingivectomy, but the condition can recur if the medications are continued.
Acute Pericoronitis
Acute inflammation of the gingiva covering the crown of an erupting tooth often occurs around the permanent lower molars. Accumulation of necrotic tissue and bacteria in the gingival sulcus facilitates an inflammatory response. A similar condition is gingival abscess, where a bacterial pocket is retained due to orthodontic appliances or prosthetic crowns. Jaw stiffness and severe pain may occur with inflammation. If not treated, it may lead to facial cellulitis and facial tissue inflammation.
The primary treatment is local intervention to remove necrotic tissue, irrigating with warm saline, and administering antibiotics. Once the acute inflammation subsides, tooth extraction or gingival surgery may be performed to prevent recurrence. Early identification of risk in lower molars and their extraction can help prevent pericoronitis in this location.
Acute Necrotizing Ulcerative Gingivitis
Acute necrotizing ulcerative gingivitis, also known as Vincent’s stomatitis or trench mouth (a disease affecting soldiers under stress in the trenches), is a type of periodontal disease characterized by spirochetes and fusobacteria in the mouth. However, it is unclear whether these bacteria cause the disease or occur secondarily. Acute necrotizing ulcerative gingivitis primarily occurs in adolescents and adults. The disease rarely occurs in healthy children in developed countries but is more common in children in southern India and some African countries, particularly among malnourished children. In these patients, lesions may extend to adjacent tissues, causing necrosis of facial tissues (necrotizing fasciitis or oral ulcers).
Clinical manifestations of acute necrotizing ulcerative gingivitis include: (1) necrosis and ulceration of gingival tissue between teeth, (2) presence of a pseudomembrane on the surface of the lesions, (3) halitosis, (4) swollen cervical lymph nodes, (5) fatigue, and (6) fever. This disease can be mistaken for herpes gingivostomatitis. Examination of necrotizing ulcerative gingivitis tissue under a dark-field microscope can reveal spirochetes.
Treatment for acute necrotizing ulcerative gingivitis is divided into two phases: Phase 1 involves the use of antibiotics (penicillin or erythromycin), cleaning necrotic tissue locally, applying hydrogen peroxide (topical application of 10% carbamide peroxide in glycerol), and administering analgesics. The disease typically resolves quickly within 48 hours of treatment. Phase 2 is necessary if the disease resolves but leaves irreversible damage to periodontal tissues.
Dr. PHAM HONG DUC
