I. TRAUMA:
II. HEREDITARY:
- Acatalasia
- Chediak-Higashi syndrome
- Chronic neutropenia
- Cyclic neutropenia
- Dentin dysplasia
- Hypophosphatasia
- Hypophosphatemic vitamin D resistant rickets
- Lesch-Nyhan syndrome
- Papillon-Lefèvre syndrome
III. NEOPLASMS:
- Lymphomas and leukemias
- Soft and hard tissue, benign and malignant, neoplasms either primary or metastatic as well as some tumor-like diseases.
IV. MISCELLANEOUS:
- Acrodynia
- Langerhans' cell histiocytosis (histiocytosis X)
- Odontodysplasia (ghost teeth)
- Osteomyelitis
- Periodontitis
- Trisomy 21 (Down's syndrome)
- Vitamin C deficiency
ACCIDENTS. The most frequent causes of premature loss of teeth are accidents especially in children. The teeth which are lost with greater frequency are the maxillary central incisors. Recent surveys indicate that 59% of patients with traumatic teeth injuries are boys and that in 63% of all cases the leading cause of trauma are falls. Traumatic injuries to teeth lead to tooth loss in 46% of cases. The majority of accidents are responsible for partial loss of teeth but severe injury to the face and/or skull can produce exfoliation and/or fractures of several teeth.
PSYCHOTIC PATIENTS. Loss of teeth in these patients is generally a consequence to improper oral hygiene. Ocasionally extractions are mandatory especially when a patient has a self-destructive behavior (see Lesch Nyhan syndrome below). Accidents also play a minor role in premature loss of teeth in psychotic patients.
RADIATION. Lymphocytes, lymphoblasts, bone marrow, epithelium of intestine and stomach and germ cells are damaged at radiation doses of =2500 r. With doses of 2500 to 5000 r the epithelium of the skin, endothelium, salivary glands, bone and cartilage, are affected. If the dose is =5000 r then serious damage and eventual destruction of kidney, liver, thyroid and other organs occur. Radiotherapy is used in the treatment of malignacies which are radiosensitive such as lymphomas or Kaposi's sarcoma among others. When malignancies of the orofacial region are treated by means of radiation one of the most common sequelae is xerostomia due to salivary gland destruction (Figure 1). Xerostomia is responsible for the development of cervical caries. Another complication is osteonecrosis which in many instances is initiated by severe periodontal involvement. Loss of teeth is the end result of these radiation secondary effects.
Figure 1. This patient had undergone radiation therapy for an adenocarcinoma of the parotid gland. Note the rampant caries and the dryness of the gingiva as a consequence to xerostomia. The right lateral incisor has been lost for that reason. Children undergoing radiation of the head and neck areas, may also develop failure or delay in tooth development and or eruption, enamel hypoplasia, microdontia and abnormal root formation. Teeth germs are highly susceptible to the effects of radiation. All these complications are responsible for premature loss of teeth.
ACATALASIA (acatalasemia, Takahara's disease). This syndrome is inherited as an autosomal recessive, the catalase gene has been mapped to the centromeric region of the short arm of chromosome 11 (11p13-14.1). Acatalasia is characterized by absence of the enzyme catalase and the majority of patients are of Japanese extraction. Acatalasemia is not the most proper name because there is also absence of the enzyme in liver, muscle and bone marrow. The enzyme catalase degrades hydrogen peroxide liberating a molecule of oxygen, which is the reason why blood bubbles when in contact with hydrogen peroxide. In these patients when food debris accumulates in the gingival sulcus or when the gingiva is injured during mastication, bacterial infection with hemolytic streptococci or pneumococci type 1 is a high possibility. These bacteria lack catalase and produce hydrogen peroxide. The peroxide destroys hemoglobin because of abcense of catalase thus depriving the infected area of oxygen and causing necrosis. Necrosed tissues favor the development of more bacteria thus establishing a vicious cycle. In extreme cases patients present progressive gangrenous gingivitis and periodontal disease with destruction of alveolar bone and loss of teeth.
CHEDIAK-HIGASHI SYNDROME. Chediak-Higashi syndrome (CHS) is inherited as an autosomal recessive, the responsible gene has been mapped to the long arm of chromosome 1 band 42.1 to 42. 2 (1q42.1-42. 2). The syndrome is characterized by pigment abnormalities, mostly oculocutaneous albinism and diffuse depigmentation of skin, abnormal neutrophil function and neutropenia which are responsible for infections, diminished chemotaxis, large abnormal lysosomal bodies and altered natural killer cell functions. Additionally the platelets in these patients have abnormal and deficient dense bodies, this component is responsible for spontaneous bleeding and easy bruising. Other components of the syndrome are photophobia, enterocolitis and peripheral neuropathy. The basic defect is a deficient secretion of myeloperoxidase by lysosomes (degranulation disorder). Prenatal diagnosis is achieved by identifying giant neutrophil granules in the fetal blood. Bone marrow transplant has been used with excellent results in several cases. Eighty five percent of children with CHS, especially those that have not undergone bone marrow transplant, develop the accelerated phase of the syndrome which is characterized by a lymphoproliferative reaction eventuating in an unusual lymphoma-like condition which generally conduces to death. The remaining 15% of patients present less severe clinical manifestations of the syndrome. The accelerated phase can be triggered by infections with lymphoproliferative viruses or the Epstein Barr virus. Most patient die during the first 10 years of life either by developing the accelerated phase, severe infections or profuse bleeding. The oral lesions are a consequence of repeated infections and they consist of ulcers, markedly hypertrophic gingivitis and severe periodontal destruction. Periodontal treatment of these patients is often unsuccessful. Due to these frequent recurrent intraoral infections there is extensive alveolar bone loss which in most patients leads to tooth exfoliation.
CHRONIC NEUTROPENIA (congenital). Chronic neutropenia is inherited as an autosomal recessive and presents similar clinical features as those observed in cyclic neutropenia but it is not periodic (vide infra). Patients with chronic neutropenia are at high risk of developing leukemia.
CYCLIC NEUTROPENIA. Cyclic neutropenia is inherited as autosomal dominant and is characterized by periodic episodes of agranulocytosis of short duration (bone marrow maturation arrest). Cyclic neutropenia is possibly due to a mutation in the human granulocyte colony stimulating factor G-CSF. The cycles occur with an interval of 21 to 27 days but in some patients may be extended to several months. The clinical manifestations are related to the lack of defense associated with the blood picture. Intraoral manifestations consist of severe acute necrotizing ulcerative gingivitis or gingivostomatitis. (Figure 2). Areas of ulceration may also be observed on the tongue and other oral mucosas. The ulcers, which are markedly painful and have a bleeding base, are deep, of variable size and have a crater-like appearance. Repeated attacks to the gingiva lead to severe periodontal disease with loss of alveolar bone, tooth mobility and exfoliation (Figure 3). The oral lesions are generally secondarily infected. These episodes of neutropenia generally persist for two to three days. When neutrophils return to normal the oral lesions tend to improve.
Figure 2. This 6 year-old girl presented with marked teeth mobility and severe periodontal disease. She had cyclic neutropenia. Her father was similarly affected.
Figure 3. These radiographs are from another child with cyclic neutropenia. Note the marked destruction of the alveolar bone.
Systemic manifestations include fever, malaise, sore throat and occasional cutaneous infections. These manifestations can be prevented first by determining the frequency of the cycles, generally 24 days, which is done by periodic neutrophil counts and then by instituting preventive antibiotic therapy to protect the patient from secondary opportunistic infections. Maintaining proper dental hygiene and periodic prophylactic cleaning of teeth, should be routine treatment in these patients.
DENTIN DYSPLASIA is inherited as autosomal dominant with complete penetrance. The enamel is normal while dentin and pulp are not. There are two varieties, type I and type II, only type I can be associated to premature loss of teeth. Type I or radicular dentin dysplasia, affects both dentitions. The morphology and color of the crown of the teeth are within normal limits. The roots on radiographs are seen as very short and with pointed ends (Figure 4).
Figure 4. These serial radiographs are from a patient with radicular dentin dysplasia. Note the markedly short and pyramidal roots. Pulp chambers are absent but in some teeth they have a half moon shape. Also note several periapical radiolucencies. Radiographs also show obliterated pulp chambers in the primary dentition and pulpal crescent shape in the permanent dentition. Periapical radiolucencies can also be seen. Teeth are lost generally due to trauma which will easely induce tooth exfoliation due to the roots' shape and length.
HYPOPHOSPHATASIA in some families is inherited as an autosomal dominant, affected individuals having a mild form of the syndrome. The majority of cases are inherited as an autosomal recessive. Hypophosphatasia is caused by a basic defect in the gene-encoding for tissue nonspecific alkaline phosphatase (TNSALP), the gene has been mapped to the short arm of chromosome 1 (1p36.1-34). TNSALP is also known as liver/bone/kidney alkaline phosphatase and in humans it hydrolyses phosphate from pyridoxal5'-phosphate, pyrophosphate and phosphoethanolamine (Figure 5). The resulting inorganic phosphate is utilized in the production of hydroxy-apatite crystals which are necessary for bone, enamel, dentin and cementum formation.
Figure 5. This schematic figure represents the mechanism by which the enzyme alkaline phosphatase hydrolyses various phosphates.
Hypophosphatasia is characterized by diminished serum levels of alkaline phosphatase and the presence in the urine of phosphoethanolamine. The infantile variety is characterized by severe rickets, hypercalcemia and failure to thrive; this form is lethal. The juvenile variety is characterized by increased propensity to infections, bone deformities, costochondral junction enlargement called rachitic rosary, failure of calvarium to calcify and GI and renal problems. Patients with this form typically present spontaneous shedding of primary teeth due to lack of cementogenesis. Almost always only the anterior primary uniradicular teeth are shed, multiradicular teeth as well as permanent teeth are not lost (Figure 6). There is no periodontal or gingival involvement, the pulp chamber of all teeth are larger than normal.
Figure 6. This child has the infantile variety of hypophosphatasia. The incisors have been lost due to lack of periodontal attachment because of lack of cementum formation.
Teeth roots are not resorbed and there is horizontal atrophy of alveolar bone due to the fact that there is no cementum to provide periodontal ligament attachment and mechanical stimulation of the alveolus. The adult form is characterized by spontaneous fractures and bone changes similar to those seen in rickets but to a minor degree.
HYPOPHOSPHATEMIC VITAMIN D RESISTANT RICKETS is inherited as an X-linked and it is characterized by hypophosphatemia (diminished amount of serum phosphorus) with decreased renal tubular resorption of inorganic phosphates, normocalcemia, minor changes suggestive of rickets, and osteomalacia not responding to vitamin D therapy. The teeth have abnormally large pulp chambers and pulp horns with microtracts that cause communication of the pulp with the oral cavity. This communication eventually produces pulpitis and consequent pulp necrosis with periapical pathology (Figure 7).
Figure 7. This is a panoramic radiograph of an adolescent with hypophosphatemic vitamin D resistant rickets. Note the various endodontic treatments due to abnormal cracks in the dentin which exposed the pulp to the oral environment.
Figure 8. This is a microscopic section of a molar from a patient with hypophosphatemic vitamin D resistant rickets. Note the large crack in the dentin extending to the dentinal enamel junction. Arrow 1 points to abnormal globular dentin and arrow 2 points to an abnormally large dentinal tubule.
Single or multiple gingival sinuses and abscesses are associated to the periapical pathology and many teeth are lost on this account due to extractions. The dentin is globular and hypocalcified presenting clefts and tubular defects (Figure 8). The cementum is also abnormal. There is no gingivitis and/or periodontitis.
LESCH-NYHAN SYNDROME is inherited as X-linked and is characterized by a deficiency of the the purine salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRTase deficiency). There are several mutations that can induce the development of the syndrome. Characterization of the HPRT mutation allows for detection of carrier and prenatal diagnosis. Affected patients have spastic cerebral palsy, mental retardation, severe motor disability, cognition, ocular motility, and behavioral control. These findings seem to point to a dysfunction of the basal ganglia. Patients have a self-mutilating aggressive behavior including mutilation of lips by constant chewing on them; as a rule the tongue is spared. Chewing of finger with resultant amputation as well as chewing of hands is also a common finding in these patients (Figure 9)
Figure 9. The photo to the left is that of a child with the Lesch-Nyhan syndrome. Note the mutilation of the lower lip and also on the index finger of his right hand. These mutilations were inflicted by self-biting. The photo to the right is the hand of another patient with the Lesch-Nyhan syndrome. Note the bite marks on the dorsum of his hand.
Teeth are lost due to prophylactic extractions in order to avoid mutilation of lips and other body parts by chewing on them. Differential diagnosis should include congenital indifference to pain.
PAPILLON-LÈFEVRE SYNDROME is inherited as autosomal recessive and is characterized by marked destruction of the periodontium (periodontoclasia) of both dentitions with premature loss of teeth and palmar and plantar hyperkeratosis. The gene has been mapped to the long arm of chromosome 11 (11q14-21). The patients are normal at birth with only reddening of palms and soles. Teeth erupt in normal sequence, position and time. At around 1 1/2 to 2 years of age a marked gingivo-periodontal inflammatory process develops with edema, bleeding, alveolar bone resorption and teeth mobility with consequent exfoliation. Concurrent with these oral lesions the palms and soles develop a red scaly keratosis that occasionally extends to the dorsal surfaces of hand and feet. The oral lesions are complicated with superimposed inflammation and radiographs reveal marked alveolar bone resorption with vertical pockets. Teeth are lost in eventually the same sequence in which they erupted. When the last tooth is lost the gingiva acquires a normal appearance. The hand and feet lesions remain as red-white, scaly, thick areas of hyperkeratinization. The permanent dentition starts to erupt also at the proper time, but around 8 to 9 years of age, the gingivo-periodontal destruction is repeated in the same manner as the primary dentition (Figure 10). All permanent teeth are lost before age 14 in the same sequence in which they erupted. After all the permanent teeth are lost (except for the third molars, which are not affected) the gingiva resumes its normal appearance.
Figure 10. This 12 year-old boy with Papillon Lefèvre syndrome presents an advanced periodontal destruction with marked gingival inflammation, root exposure and teeth mobility. His palms and soles were markedly hyperkeratotic.
Figure 11. This panoramic radiograph is from another patient with the Papillon Lefèvre syndrome. Note the vertical periodontal pockets and exfoliation of teeth, even those which roots are still being formed. (From Sedano HO, Saulk JJ, Gorlin RJ: Oral Manifestations of Inherited Disorders. Boston, Butterworth, 1977, with permission.)
The basic defect for
this syndrome is unknown. Peripheral blood neutrophil chemotaxis have
been reported to be depressed in patients with Papillon-Lefèvre syndrome.
This decreased chemotaxis suggests that neutrophils may be an important
factor in the etiology of the periodontal destruction in patients with
this syndrome. Current research suggests a bacterial and viral involvement
as the initiating factors for the periodontal destruction that occurs
in this syndrome. It has been suggested that the genetic component of
Papillon Levefèvre syndrome is a predisposition rather than the main determinant
of periodontal disease.
Most therapeutic attempts of the oral lesions have been unsuccessful.
Various treatments have been attempted with partial success but the number
of cases with successful long term follow up is limited. Prevention of
tooth loss in some patients with the syndrome has been partially obtained
with initial periodontal treatment followed by a carefully monitored oral
hygiene program and the use of ultrasonic scaling. Still other treatments
have consisted of extraction of the periodontally affected deciduous teeth
under amoxycillin and clavulanic acid coverage followed by a highly regimented
oral hygiene program of the permanent teeth. Edentulous patients tolerate
full dentures well and oseo-integrated implants have been utilized in
a few cases. The skin manifestations remain for life, but treatment with
Retinoids (oral etretinate) has proven to be efficient in controlling
the hyperkeratinization. These patients do not have any other abnormalities.
The differential diagnosis should include: Haim-Munk syndrome (congenital
keratosis palmo-plantaris, progressive periodontal disease, arachnodactyly,
deformed fingers) and also hyperkeratosis palmo-plantaris and attached
gingival hyperkeratosis.
LEUKEMIA is a disease characterized by the appearance of immature neoplastic white blood cells in the circulation. A virus may be the probable cause, but is as yet not proven. Oral lesions in leukemia are characterized by hyperplastic gingivitis with a cyanotic bluish-red discoloration (Figure 12). The lesions vary in degree and severity. In some patients there is diffuse enlargement of the gingiva. The oral tissues are friable and bleed easily (Figure 13). Frequently, hyperplastic gingivae may completely cover the teeth.
Figure 12. Note the marked hypertrophic gingivitis in this child with leukemia. Failure to maintain proper oral hygiene in patients with leukemia can conduce to premature loss of teeth.
Figure 13. This adult female was also affected with leukemia. Note the marked hypertrophy of the interdental papillae as well as the large hematomas in the lower lip.
In severe cases, purpuric
lesions and necrotic ulcers of the oral mucous membranes are also seen.
A noma-like complication may be associated with terminal cases of leukemia
owing to lack of tissue defense against a minor irritant. Alveolar bone
destruction and necrosis of the periodontal ligament may occasionally
lead to loosening and exfoliation of teeth. Acute necrotizing ulcerative
gingivitis may also be present. The oral manifestations of leukemia result
from both the basic systemic defect and local irritants. When the oral
cavity is kept free of local irritants such as plaque, food debris, ill-fitting
dentures, and the like, oral involvement may be minimal. The course and
complications of the disease depend upon the basic systemic defect. The
condition often has a fatal outcome.
Other blood dyscrasias, as well as advanced periodontitis, necrotizing
ulcerative gingivostomatitis, hyperplastic gingivitis, and noma, should
be considered in the differential diagnosis.
The use of complete blood count and differential establishes the diagnosis.
Gingival biopsy is only suggestive of the condition and must be corroborated
by hematologic examination. The treatment is systemic and mostly paliative
encompassing a variety of means such as chemotherapy, radiation, bone
marrow transplant, and some others. The oral cavity should be free of
local irritants and the patient must be instructed to maintain a high
level of oral hygiene.
SOFT AND HARD TISSUE NEOPLASMS. A vast number of either benign or malignant neoplasms as well as several tumor like conditions developing in the soft or hard tissues in the vicinity of teeth can be responsible for the partial loss of teeth either by directly interfering with tooth development or as a consequence to therapy. Examples include: neuroectodermal tumor of infancy (Figure 14), central giant cell granuloma, fibrous dysplasia, sarcomas, etc. (Figure 15)
Figure 14. This infant had a neuroectodermal tumor of infancy. The radiograph shows a large osteolitic lesion which is displacing teeth germs. Surgical treatment of this neoplasm also implicated ablation of those germs with permanent loss of the primary and permanent teeth affected.
Figure 15. This 38 year-old man was presented with a growth that involved the alveolar ridge, buccal gingiva and buccal mucosa. Biopsy showed this neoplasm to be a fibrosarcoma. Two molars in the area were lost due to extreme mobility. A bone sequestrum is evident.
ACRODYNIA (Pink disease, Feer's Syndrome, Raw-beef Hands and Feet). This disease rarely seen today is caused by mercurial poisoning. In the past it was generally due to mercury used in teething powders or other medications. Chardon in 1830 first described this disease and coined the name acrodynia. Mercury was suggested as an etiologic factor by several authors in the European and American literature and the symptoms of acrodynia were explained based on an interaction of vitamin B6, essential fatty acids and mercury binding to sulfhydryl groups. Clinically it is characterized by skin changes, central nervous system involvement and marked gingivostomatitis with consequent teeth exfoliation.
LANGERHANS' CELL HISTIOCYTOSIS is possibly a neoplastic proliferation of Langerhans' histiocytes which is presently classified as follows: ACUTE DISSEMINATED (Letterer-Siwe disease) it exclusively affects infants and it manifests clinically with hepatosplenomegaly and diffuse radiolucent bone lesions. The bone lesions in the jaws produce alveolar bone resorption with consequent teeth and/or teeth germs exofoliation. Radiographically this finding has been described as "floating teeth". There is also marked gingivitis and soft tissue necrosis. This type is generally fatal (Figure 16).
Figure 16. This three month-old baby was seen because of early exfoliation of teeth. A biopsy of the gingiva adjacent to the mandibular incisors rendered the diagnosis of Langerhans's cell histiocytosis. This child developed the acute disseminated variety.
CHRONIC DISSEMINATED (Hand-Schüller-Christian disease) This type usually starts after 5 or 6 years of age and it is characterized by exfoliation of teeth and bone radiolucencies due to intrabony lesions (Figure 17). One of the typical findings is the so-called "geographic skull" due to the presence of lesions throughout the cranium. Retro-orbital lesions produce exophthalmos and lesions in the tuber cinerium cause diabetes insipidus. This type generally has a long and benign course.
Figure 17. This serial intraoral radiograph is of a boy with Langerhans's cell histiocytosis chronic disseminated variety. Note the floating teeth appearance and the marked alveolar bone destruction.
CHRONIC FOCAL (Eosinophilic granuloma of the bone) is the localized type and when in the mandible it produces mobility and exfoliation of teeth. It generally affects individuals after 20 years of age. Teeth are generally lost because of extraction due to mobility induced by the bone lesions. Histologically the three varieties share the marked proliferation of Langerhans' histiocytes and a profuse eosinophil infiltrate with localized areas of necrosis. An incisional biopsy of the affected gingiva will render the diagnosis.
ODONTODYSPLASIA (ghost teeth). This rare malformation of teeth affects enamel dentin pulp and cementum formation of a group of teeth or a quadrant of the jaw bones. The permanent teeth are affected more frequently then the primary teeth. Affected teeth are poorly mineralized and on radiographs they appear evanescent, hence the name ghost teeth (Figure 18). They generally fail to erupt but if they do they have the consistency of gelatin. They need to be extracted. The actual causing agent is unknown even if circulatory disturbances, nutritional deficiencies, genetics and viral causes, among others, have been cited as possible etiology.
Figure 18. The photo to the left represents an example of regional odontodysplasia. Note the abnormal morphology of the central and lateral right incisors as well as the right canine. This intraoral radiograph to the right shows the appearance of ghost teeth. Note the lack of proper calcification of enamel, dentin and cementum. Also note the abnormal pulp chamber and root shape.
OSTEOMYELITIS. Osteomyelitis
constitutes an acute or chronic inflammation of bone marrow. A variety
of pyogenic organisms may be responsible. Acute osteomyelitis is characterized
by pus in the bone marrow, necrosis and sequestration of bone, peripheral
sclerosis of bone and subperiosteal proliferation of bone. The pus penetrates
the bone to drain through multiple sinuses. Chronic osteomyelitis may
be a prolongation of acute inflammatory process over many years, with
death of bone and sequestration which is difficult to eradicate. A variety
of osteomyelitis, chronic sclerosing osteomyelitis, is characterized by
a subacute inflammation of the bone marrow and sclerosis of the bone.
A rare form of acute osteomyelitis occurs in infants and young children.
It is of hematogenous origin and affects the alveolar process of the maxilla,
frequently with multiple discharging sinuses around the deciduous teeth
and discharging through the periodontal membrane. In adults, the mandible
is more frequently involved, presenting as an acute painful swelling with
fever and cervical lymphadenopathy. Pus may discharge from sinuses in
the buccal sulcus. A nonvital, tender tooth with a periapical abscess
may be the cause, and fractures of the jaws are equally involved. Anesthesia
or paresthesia of the inferior dental nerve may be found. Radiographically,
the lesion shows as a diffuse radiopacity with focal areas of bone sclerosis
indicating sequestration. Osteomyelitis may develop in patients whose
bone pattern is abnormal for any reason, for example, with osteopetrosis,
cemental dysplasias, Paget disease of bone and radionecrosis. The chronic
suppurative osteomyelitis is frequently very resistant to treatment, and
large areas may be lost by sequestration.
Radiographically the "moth-eaten" appearance is quite characteristic.
Nevertheless, Paget disease of bone, cemental and fibrous dysplasias should
be considered in the differential diagnosis. The cause of the process
should also be established in order to institute proper diagnosis. Osteomyelitis
of such unusual causes such as tuberculosis could affect the jaws or also
some more common conditions such as actinomycosis. In any form of osteomyelitis
teeth can be lost due to the severe bone loss and necrosis (Figure 19)
or because of necessary extractions.
Figure 19. This photo shows a patient with osteomyelitis. The left side depicts the intraoral appearance and the right side is the sequestrum that involved three teeth and their adjacent tissues.
Pus should be sent for smear and culture. The white blood count is frequently elevated, as well as the erythrosedimentation rate. High doses of antibiotics prescribed for a prolonged period of time are the necessary treatment. Excision of sequestra, extraction of affected teeth and curetting of the affected bone may encourage healing. Fractures must be fixed rigidly.
PERIODONTITIS. The American Academy of Periodontology has classified periodontitis as:
- Adult periodontitis
- Early-onset periodontitis
a. Prepubertal periodontitis
b. Juvenile periodontitis
i. Localized
ii. Generalized
c. Rapidly progressive periodontitis -
Periodontitis associated with systemic disease
-
Necrotizing ulcerative periodontitis
-
Refractory periodontitis
Here only the early-onset
periodontitis wil be briefly discussed. Before the diagnosis of early-onset
periodontitis is established all the possible systemic causes of premature
loss of attachment with consequent teeth exfoliation will need to be excluded.
These varieties of periodontitis are considered not to be associated with
the presence of plaque and calculus but with deficiencies in the immune
system and possible genetic predispositions. A great number of epidemiological
studies have shown that young adults and children may develop severe periodontal
disease that could induce premature loss of primary and/or succedaneous
teeth. In 1987 it was reported that the prevalence of early-onset periodontitis
in adolescents was estimated at about 10% in African-American, 5% in Hispanics
and 1.3% in white adolescents.
Prepubertal periodontitis occurs in young children, mostly girls, with
onset at around 4 years of age. It is localized to few primary teeth and
it may eventuate in juvenile periodontitis. Recently a gene of major effect
for prepubertal periodontitis has been mapped to chromosome 11q14 in a
consanguineous Jordanian family, the parents were first cousins, This
candidate gene overlaps the region of chromosome 11q14 that contains the
cathepsin C gene responsible for Papillon-Lefèvre and Haim-Munk syndromes.
The localized variety of juvenile periodontitis (LJP) begins around the early years of the second decade of life (10 to 13 years old) and it generally affects molars and incisors. Around 70% of patients with LJP have been found to have abnormal neutrophil functions characterized by diminished phagocytosis and chemotaxis as well as reduced protein kinase C (PKC) activity, and reduced calcium entry. Several reports indicate a high familial preponderance. Clinically there is not much accumulation of supragingival plaque and/or calculus, the gingiva is almost normal in appearance and there is minimal subgingival plaque deposition. Radiographs show marked destruction of alveolar bone with vertical pocket formation (Figure 20). Advanced cases present teeth mobility and malposition which may lead to teeth loss.
Figure 20. These radiographs are from a 29 year-old man with early onset periodontitis. Note the marked vertical pockets and the alveolar bone destruction at the level of the furcation. This patient had presented the first manifestations of his periodontal involvement during his second decade of life.
The generalized variety of juvenile periodontitis is considered by some authors as a wider manifestation of LJP. Patients are generally above 13 years of age and all teeth may be affected. Similar to LJP there is not much accumulation of supragingival plaque and/or calculus. Either variety may lead to premature loss of teeth.
TRISOMY 21. Down syndrome, is the most frequent of the trisomies. The facies are characterized by slanted eyes. Patients are generally shorter than normal and present a wide range of intelligence level, from near normal to marked retardation. Gingivo-periodontal disease has been reported in ninety percent of affected children. Premature loss of teeth, especially the central mandibular incisors, is frequently observed due to alveolar bone loss. Hypodontia and abnormally shaped teeth are also present in patients with trisomy 21. Heart abnormalities are present in over 30% of affected individuals. Ninety five percent of cases of Down syndrome are a consequence to chromosomal nondisjunction mostly associated with late maternal age at time of conception.
VITAMIN C DEFICIENCY.
Scurvy is the result of insufficient intake of vitamin C. Humans cannot
synthesize vitamin C which is needed for several metabolic processes such
as intracellular oxidation and facilitation of iron intake in the GI tract.
The participation of vitamin C in collagen formation is well known and
its diminished intake will affect bone, dentin and connective tissue formation.
The recommended daily dose for vitamin C for adult nonsmoking men and
women is 60 mg/d, which is based on a mean requirement of 46 mg/d to prevent
scurvy. Recently it has been shown that by increasing the daily dose there
is a diminished possibility of acquiring some diseases such as cardiovascular
disorders, cancer and other chronic ailments, possibly due to the antioxidant
capabilities of vitamin C.
Scurvy was quite prevalent in the past but it is still occasionally observed
especially in individuals who live in isolation, alcoholics, psychotic
patients, children living in extreme poverty or individuals who lack proper
nutrition. The clinical manifestations are only apparent after prolongued
periods of diminished intake. One of the earliest systemic symptoms is
fatigue and skin hematomas due to capillary fragility, especially of the
lower extremities (Figure 21). This finding, together with gingival hemorrage
and mucosal echymoses could lead to the misdiagnosis of a blood dyscrasia,
especially leukemia. Other findings include follicular hyperkeratosis,
edema of the legs, delayed and inefficient wound healing and anemia. Intraoral
lesions are observed in dentulous patients and are characterized by gingival
hemorrhages and hypertrophy (Figure 22) as well as mucosal parlor. Destruction
of the periodontal attachment will lead to teeth mobility and alveolar
bone resorption with consequent teeth exfoliation. These oral changes
are seen in the late stages of prolongued vitamin C deficiency.
Figure 21. Note the marked hematomas due to capillary hemorrhages in the legs of the patient with scurvy shown in Figure 22.
Figure 22. This markedly hyperthrophic and hemorrhagic gingiva was seen in a patient with scurvy. She was a loner and only ate plants that she gathered in the wild. Teeth were markedly mobile.
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ACCIDENTS
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RADIATION
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Ansari G, Reid JS. Dentinal dysplasia type I: review of the literature and report of a family. Asdc J Dent Child 1997;64:429-34.
Shankly PE; Mackie IC; Sloan P. Dentinal dysplasia type I: report of a case. Internat J Paed Dent 1999;9:37-42.
Vieira AR, Modesto A, Cabral MG. Dentinal dysplasia type I: report of an atypical case in the primary dentition. Asdc J Dent Child 1998;65:141-4.
HYPOPHOSPHATASIA
Orimo H et al. Detection of deletion 1154-1156 hypophosphatasia mutation using TNSALP exon amplification. Genomics 1997;42:364-6.
Sato S, Matsuo N. Genetic analysis of hypophosphatasia. Acta Paed Japon 1997;39:528-32.
HYPOPHOSPHATEMIC VITAMIN D RESISTANT RICKETS
Murayama T et al. Familial hypophosphatemic vitamin D-resistant rickets: dental findings and histologic study of teeth.
Oral Surg Oral Med Oral Pathol Oral Radiol Endodont 2000;90:310-6.
LESCH-NYHAN SYNDROME
Nyhan WL. The recognition of Lesch-Nyhan syndrome as an inborn error of purine metabolism. J Inherit Metabol Dis 1997;20:171-8.
Rashid N, Yusuf H. Oral self-mutilation by a 17-month-old child with Lesch-Nyhan syndrome. Internat J Paed Dent 1997;7:115-7.
PAPILLON-LEFEVRE SYNDROME
Firatli E et al. Papillon-Lefèvre syndrome. Analysis of neutrophil chemotaxis. J Periodontol 1996;67:617-20.
Firatli E et al. Clinical and immunological findings in 2 siblings with Papillon-Lefèvre syndrome. J Periodontol 1996;67:1210-5.
Laass MW et al. Localisation of a gene for Papillon-Lefèvre syndrome to chromosome 11q14-q21 by homozygosity mapping. Human Genet 1997;101:376-82.
Lundgren T et al. Systemic retinoid medication and periodontal health in patients with Papillon-Lefèvre syndrome. J Clin Periodontol 1996;23:176-9.
Tinanoff N, Tempro P, Maderazo EG. Dental treatment of Papillon-Lefèvre syndrome: 15-year follow-up. J Clin Periodontol 1995;22:609-12. Velazco CH et al. Microbiological features of Papillon-Lefèvre syndrome periodontitis. J Clin Periodontol,1999;26:622-7.
NEOPLASMS and LEUKEMIA
Baliga AM et al. Oral mucosal lesions in patients with acute leukemias and related disorders due to cytotoxic therapy. J Indian Soc Pedo Prevent Dent 1995;13:25-9.
Rees TD et al. Periodontal considerations in the management of the cancer patient. J Periodontol 1997;68:791-801.
ACRODYNIA
Chardon F. De l'acrodynie. Rev méd franç 1830;3:51-74.
Martin MD et al. Spontaneous exfoliation of teeth following severe elemental mercury poisoning: case report and histological investigation for mechanism. Oral Surg Oral Med Oral Pathol Oral Radiol Endodont 1997;84:495-501.
LANGERHANS' CELL HISTIOCYTOSIS
Piattelli A, Paolantonio M. Eosinophilic granuloma of the mandible involving the periodontal tissues. A case report. J Periodont 1995;66:731-6.
Saunders JG et al. Langerhans cell histiocytosis presenting as bilateral eosinophilic granulomata in the molar region of the mandible. A case report. J Clin Periodont 1998;25:340-2.
Unlu F et al. Multifocal eosinophilic granuloma with sequential periodontitis-like lesions. J Clin Periodont 1997;24:384-7.
ODONTODYSPLASIA
Ansari Get al. Regional odontodysplasia: report of four cases. Internat J Paed Dent 1997;7:107-13.
Gerlach RF et al. Regional odontodysplasia. Report of two cases Oral Surg Oral Med Oral Pathol Oral Radiol Endodont 1998;85:308-13.
Rohanizadeh R et al. Ultrastructural organization and microanalysis studies of deciduous enamel crystallites in regional odontodysplasia (RO). J Oral Pathol Med 1998;27:501-7.
OSTEOMYELITIS
Walton AG et al. Meningococcal septicemia and disseminated intravascular coagulation affecting the premaxillary permanent tooth germs. Asdc J Dent Child 1998;65:191-3.
Hovi L et al. Opportunistic osteomyelitis in the jaws of children on immunosuppressive chemotherapy. J Ped Hematol/Oncol 1996;18:90-4.
PERIODONTITIS
Albandar JM, Brown LJ, Loe H. Clinical features of early-onset periodontitis. JAMA 1997;128:1393-9.
Delaney JE, Kornman KS. Microbiology of subgingival plaque from children with localized prepubertal periodontitis. Oral Microbiol Immunol 1987;2:71-6.
Hart TC et al. Localisation of a gene for prepubertal periodontitis to chromosome 11q14 and identification of a cathepsin C gene mutation. J Med Genet 2000;37:95-101.
Leino L, Hurttia H. A potential role of an intracellular signaling defect in neutrophil functional abnormalities and promotion of tissue damage in patients with localized juvenile periodontitis. Clinic Chemist Lab Med 1999;37:215-22.
Shapira L et al. Possible autosomal-dominant inheritance of prepubertal periodontitis in an extended kindred. J Clin Periodontol 1997;24:388-93.
Shibata K et al. Defective calcium influx factor activity in neutrophils from patients with localized juvenile periodontitis. J Periodontol 2000; 71: 797-802.
Tonetti MS, Mombelli A. Early-onset periodontitis. Annals Periodontol 1999;4:39-53.
TRISOMY 21 (DOWN'S SYNDROME)
Cichon P et al. Early-onset periodontitis associated with Down's syndrome-clinical interventional study.
Annals Periodontol 1998;3:370-80.
Sohoel DC et al. Expression of HLA class II antigens in marginal periodontitis of patients with Down's syndrome. Europ J Oral Sci 1995;103:207-13.
VITAMIN C DEFICIENCY
Carr AC, Frei B. Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. Amer J Clin Nutr 1999;69:1086-107.
Hirschmann JV, Raugi GJ. Adult scurvy. J Amer Acad Derm 1999;41:895-906
Sasaki G et al. Confluent ecchymoses on the lower extremities of a malnourished patient. J Derm 1999;26:399-401.
Tamura Y et al. Scurvy presenting as painful gait with bruising in a young boy. Arch Ped Adoles Med 2000;154:732-5.
Touyz LZ. Oral scurvy and periodontal disease. J Canad Dent Assoc 1997;63:837-45. 41.
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