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Premature loss of teeth

MedGen UID:
66678
Concept ID:
C0232513
Finding; Finding
Synonyms: Early loss of teeth; Early teeth loss; Early tooth loss; Premature tooth loss
SNOMED CT: Premature tooth loss (42756003)
 
HPO: HP:0006480

Definition

Exfoliation of a tooth more than 2 SD earlier than the normal age for the deciduous teeth and not related to traume or neglect. Exfoliation of a permanent tooth is per se abnormal. [from HPO]

Term Hierarchy

Conditions with this feature

Papillon-Lefèvre syndrome
MedGen UID:
45306
Concept ID:
C0030360
Disease or Syndrome
Papillion-Lefevre syndrome (PALS) is an autosomal recessive disorder characterized by palmoplantar keratoderma, periodontitis, and premature loss of dentition (summary by Lefevre et al., 2001).
Ehlers-Danlos syndrome, type 4
MedGen UID:
82790
Concept ID:
C0268338
Disease or Syndrome
Vascular Ehlers-Danlos syndrome (vEDS) is characterized by arterial, intestinal, and/or uterine fragility; thin, translucent skin; easy bruising; characteristic facial appearance (thin vermilion of the lips, micrognathia, narrow nose, prominent eyes); and an aged appearance to the extremities, particularly the hands. Vascular dissection or rupture, gastrointestinal perforation, or organ rupture are the presenting signs in most adults with vEDS. Arterial rupture may be preceded by aneurysm, arteriovenous fistulae, or dissection but also may occur spontaneously. The majority (60%) of individuals with vEDS who are diagnosed before age 18 years are identified because of a positive family history. Neonates may present with clubfoot, hip dislocation, limb deficiency, and/or amniotic bands. Approximately half of children tested for vEDS in the absence of a positive family history present with a major complication at an average age of 11 years. Four minor diagnostic features – distal joint hypermobility, easy bruising, thin skin, and clubfeet – are most often present in those children ascertained without a major complication.
Hyperphosphatasemia with bone disease
MedGen UID:
75678
Concept ID:
C0268414
Disease or Syndrome
Paget disease of bone-5 is an autosomal recessive, juvenile-onset form of Paget disease, a disorder of the skeleton resulting from abnormal bone resorption and formation. Clinical manifestations include short stature, progressive long bone deformities, fractures, vertebral collapse, skull enlargement, and hyperostosis with progressive deafness. There is phenotypic variability, with some patients presenting in infancy, while others present later in childhood (summary by Naot et al., 2014). For discussion of genetic heterogeneity of Paget disease of bone, see 167250.
Naegeli-Franceschetti-Jadassohn syndrome
MedGen UID:
91010
Concept ID:
C0343111
Disease or Syndrome
Naegeli-Franceschetti-Jadassohn syndrome (NFJS) is a rare autosomal dominant disorder of skin, hair, and teeth. It is characterized by complete absence of dermatoglyphics (fingerprint lines), a reticulate pattern of skin hyperpigmentation that tends to disappear with age, thickening of the palms and soles (palmoplantar keratoderma), and decreased sweating. Dental anomalies including enamel defects, skin blistering, and nail dystrophy have been reported in some patients. It can be distinguished from dermatopathia pigmentosa reticularis (DPR) by the latter's features of lifelong persistence of the skin hyperpigmentation, partial alopecia, and absence of dental anomalies (summary by Lugassy et al., 2006).
Dysosteosclerosis
MedGen UID:
98150
Concept ID:
C0432262
Disease or Syndrome
A rare genetic primary bone dysplasia disease characterized by progressive osteosclerosis and platyspondyly.
Familial expansile osteolysis
MedGen UID:
96593
Concept ID:
C0432292
Congenital Abnormality
Familial expansile osteolysis is an autosomal dominant bone dysplasia characterized by increased bone remodeling with osteolytic lesions mainly affecting the appendicular skeleton. There is medullary and cortical expansion of the bone without sclerosis, leading to painful and disabling deformities and tendency to pathologic fracture. Clinical features include onset of conductive hearing loss in childhood, premature loss of teeth, and variably increased serum alkaline phosphatase (summary by Palenzuela et al., 2002 and Elahi et al., 2007).
Oculodentodigital dysplasia
MedGen UID:
167236
Concept ID:
C0812437
Congenital Abnormality
Oculodentodigital syndrome is characterized by a typical facial appearance and variable involvement of the eyes, dentition, and fingers. Characteristic facial features include a narrow, pinched nose with hypoplastic alae nasi, prominent columella and thin anteverted nares together with a narrow nasal bridge, and prominent epicanthic folds giving the impression of hypertelorism. The teeth are usually small and carious. Typical eye findings include microphthalmia and microcornea. The characteristic digital malformation is complete syndactyly of the fourth and fifth fingers (syndactyly type III) but the third finger may be involved and associated camptodactyly is a common finding (summary by Judisch et al., 1979). Neurologic abnormalities are sometimes associated (Gutmann et al., 1991), and lymphedema has been reported in some patients with ODDD (Brice et al., 2013). See review by De Bock et al. (2013). Genetic Heterogeneity of Oculodentodigital Syndrome An autosomal recessive form of ODDD (257850) is also caused by mutation in the GJA1 gene, but the majority of cases are autosomal dominant.
Hajdu-Cheney syndrome
MedGen UID:
182961
Concept ID:
C0917715
Disease or Syndrome
Hajdu-Cheney syndrome (HJCYS) is a rare autosomal dominant skeletal disorder characterized by short stature, coarse and dysmorphic facies, bowing of the long bones, and vertebral anomalies. Facial features include hypertelorism, bushy eyebrows, micrognathia, small mouth with dental anomalies, low-set ears, and short neck. There is progressive focal bone destruction, including acroosteolysis and generalized osteoporosis. Additional and variable features include hearing loss, renal cysts, and cardiovascular anomalies (summary by Ramos et al., 1998; Simpson et al., 2011; Isidor et al., 2011).
Dyskeratosis congenita, X-linked
MedGen UID:
216941
Concept ID:
C1148551
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Mandibuloacral dysplasia with type B lipodystrophy
MedGen UID:
332940
Concept ID:
C1837756
Disease or Syndrome
Mandibuloacral dysplasia with type B lipodystrophy (MADB) is a rare autosomal recessive disorder characterized by postnatal growth retardation, craniofacial anomalies such as mandibular hypoplasia, skeletal anomalies such as progressive osteolysis of the terminal phalanges and clavicles, and skin changes such as mottled hyperpigmentation and atrophy. The lipodystrophy is characterized by generalized loss of subcutaneous fat involving the face, trunk, and extremities. Some patients have a progeroid appearance. Metabolic complications associated with insulin resistance have been reported (Schrander-Stumpel et al., 1992; summary by Simha et al., 2003). For a general phenotypic description of lipodystrophy associated with mandibuloacral dysplasia, see MADA (248370).
XFE progeroid syndrome
MedGen UID:
410064
Concept ID:
C1970416
Disease or Syndrome
An autosomal recessive condition caused by mutation(s) in the ERCC4 gene, encoding DNA repair endonuclease XPF. it is characterized by characterized by cutaneous photosensitivity and progeroid features in multiple organ systems.
Candidiasis, familial, 1
MedGen UID:
414015
Concept ID:
C2751429
Disease or Syndrome
Chronic mucocutaneous candidiasis (CMC) includes a group of rare disorders with altered immune responses, selective against Candida, characterized by persistent and/or recurrent infections of the skin, nails, and mucous membranes, caused by organisms of the genus Candida, mainly Candida albicans (Zuccarello et al., 2002). Isolated familial chronic mucocutaneous candidiasis is distinct from candidiasis with endocrinopathy (240300). In myeloperoxidase deficiency (254600), susceptibility to candidiasis may be increased. Genetic Heterogeneity of Candidiasis Familial candidiasis-1 (CANDF1) maps to chromosome 2p. CANDF2 (212050) is caused by mutation in the CARD9 gene (607212) on chromosome 9q34.3. CANDF3 (607644), a form restricted to nails of the hands and feet, maps to chromosome 11. CANDF4 (613108) is caused by mutation in the CLEC7A gene (606264) on chromosome 12p13. CANDF6 (613956) is caused by mutation in the IL17F gene (606496) on chromosome 6p12. CANDF7 (614162) is caused by mutation in the STAT1 gene (600555) on chromosome 2q32. CANDF8 (615527) is caused by mutation in the TRAF3IP2 gene (607043) on chromosome 6q21. CANDF9 (616445) is caused by mutation in the IL17RC gene (610925) on chromosome 3p25. A form of familial candidiasis, previously thought to be isolated and designated CANDF5, has been found to be part of a primary immune deficiency (IMD51; 613953) that includes Staphylococcal skin infections and increased susceptibility to chronic bacterial respiratory infections.
Metaphyseal dysplasia-maxillary hypoplasia-brachydacty syndrome
MedGen UID:
762788
Concept ID:
C3549874
Disease or Syndrome
Metaphyseal dysplasia and maxillary hypoplasia with or without brachydactyly (MDMHB) is an autosomal dominant bone dysplasia characterized by metaphyseal flaring of long bones, enlargement of the medial halves of the clavicles, maxillary hypoplasia, variable brachydactyly, and dystrophic teeth (summary by Moffatt et al., 2013).
Chronic familial neutropenia
MedGen UID:
777137
Concept ID:
C3665676
Disease or Syndrome
Paget disease of bone 2, early-onset
MedGen UID:
899166
Concept ID:
C4085251
Disease or Syndrome
Paget disease is a metabolic bone disease characterized by focal abnormalities of increased bone turnover affecting one or more sites throughout the skeleton, primarily the axial skeleton. Bone lesions in this disorder show evidence of increased osteoclastic bone resorption and disorganized bone structure. See reviews by Ralston et al. (2008) and Ralston and Albagha (2014). For a discussion of genetic heterogeneity of Paget disease of bone, see 167250.
Dyskeratosis congenita, autosomal recessive 6
MedGen UID:
905452
Concept ID:
C4225356
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Ehlers-Danlos syndrome, periodontal type 1
MedGen UID:
1642148
Concept ID:
C4551499
Disease or Syndrome
Periodontal Ehlers-Danlos syndrome (pEDS) is characterized by distinct oral manifestations. Periodontal tissue breakdown beginning in the teens results in premature loss of teeth. Lack of attached gingiva and thin and fragile gums lead to gingival recession. Connective tissue abnormalities of pEDS typically include easy bruising, pretibial plaques, distal joint hypermobility, hoarse voice, and less commonly manifestations such as organ or vessel rupture. Since the first descriptions of pEDS in the 1970s, 148 individuals have been reported in the literature; however, future in-depth descriptions of non-oral manifestations in newly diagnosed individuals with a molecularly confirmed diagnosis of pEDS will be important to further define the clinical features.
Periodontitis, aggressive 1
MedGen UID:
1644602
Concept ID:
C4551681
Disease or Syndrome
Aggressive periodontitis, which may be generalized or localized, is characterized by severe and protracted gingival infections, leading to tooth loss. Amounts of microbial deposits are generally inconsistent with the severity of periodontal tissue destruction and the progression of attachment and bone loss may be self arresting (American Academy of Periodontology, 2000). The term 'aggressive periodontitis' replaced the terms 'early-onset,' 'prepubertal,' or 'juvenile periodontitis' at a 1999 International workshop for a classification of periodontal disease and conditions, where it was decided that the classification terminology should not be age dependent or require knowledge of rates of progression (Armitage, 1999). Genetic Heterogeneity of Aggressive Periodontitis Aggressive periodontitis-2 (608526) has been mapped to chromosome 1q25.
Dyskeratosis congenita, autosomal dominant 1
MedGen UID:
1645250
Concept ID:
C4551974
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Osteopetrosis, autosomal dominant 3
MedGen UID:
1648454
Concept ID:
C4748197
Disease or Syndrome
Autosomal dominant osteopetrosis-3 (OPTA3) is characterized by phenotypic variability. Some patients have typical features of osteopetrosis, including fractures after minor trauma, early tooth loss, anemia, hepatosplenomegaly, and a generalized increase in bone mineral density, whereas other patients exhibit localized osteosclerosis and generalized osteopenia. OPTA3 represents a relatively malignant form of osteopetrosis in some patients who develop significant pancytopenia and hepatosplenomegaly (Bo et al., 2016). For a discussion of genetic heterogeneity of autosomal dominant osteopetrosis, see OPTA1 (607634).
Cancer, alopecia, pigment dyscrasia, onychodystrophy, and keratoderma
MedGen UID:
1678330
Concept ID:
C5193062
Disease or Syndrome
CAPOK syndrome (CAPOK) is characterized by onset of symptoms in the first year of life, with the development of progressive alopecia, hypo- and hyperpigmented macular skin lesions, palmoplantar keratoderma, and nail dystrophy. Beginning in the third decade of life, patients develop recurrent squamous cell carcinomas. Some patients may have brittle teeth resulting in tooth loss, and multinodular goiter has been observed (Courcet et al., 2015).
Mandibuloacral dysplasia with type A lipodystrophy
MedGen UID:
1757618
Concept ID:
C5399785
Disease or Syndrome
Mandibuloacral dysplasia with type A lipodystrophy (MADA) is an autosomal recessive disorder characterized by growth retardation, craniofacial anomalies with mandibular hypoplasia, skeletal abnormalities with progressive osteolysis of the distal phalanges and clavicles, and pigmentary skin changes. The lipodystrophy is characterized by a marked acral loss of fatty tissue with normal or increased fatty tissue in the neck and trunk. Some patients may show progeroid features. Metabolic complications can arise due to insulin resistance and diabetes (Young et al., 1971; Simha and Garg, 2002; summary by Garavelli et al., 2009). See also MAD type B (MADB; 608612), which is caused by mutation in the ZMPSTE24 gene (606480).
Odontochondrodysplasia 2 with hearing loss and diabetes
MedGen UID:
1782909
Concept ID:
C5543275
Disease or Syndrome
Odontochondrodysplasia-2 with hearing loss and diabetes (ODCD2) is characterized by growth retardation with proportionate short stature, dentinogenesis imperfecta, sensorineural hearing loss, insulin-dependent diabetes, and mild intellectual disability (Cauwels et al., 2005; Lekszas et al., 2020). For a discussion of genetic heterogeneity of ODCD, see ODCD1 (184260).

Professional guidelines

PubMed

Khan AA, Josse R, Kannu P, Villeneuve J, Paul T, Van Uum S, Greenberg CR
Osteoporos Int 2019 Sep;30(9):1713-1722. Epub 2019 Mar 26 doi: 10.1007/s00198-019-04921-y. PMID: 30915507
López-Gómez SA, Villalobos-Rodelo JJ, Ávila-Burgos L, Casanova-Rosado JF, Vallejos-Sánchez AA, Lucas-Rincón SE, Patiño-Marín N, Medina-Solís CE
Sci Rep 2016 Feb 26;6:21147. doi: 10.1038/srep21147. PMID: 26916132Free PMC Article
Ashri NY
J Int Acad Periodontol 2008 Jul;10(3):81-6. PMID: 18714933

Recent clinical studies

Etiology

Dommisch H, Walter C, Difloe-Geisert JC, Gintaute A, Jepsen S, Zitzmann NU
J Clin Periodontol 2022 Jun;49 Suppl 24:149-166. Epub 2021 Dec 1 doi: 10.1111/jcpe.13563. PMID: 34854115
Fenn JS, Lorde N, Ward JM, Borovickova I
J Clin Pathol 2021 Oct;74(10):635-640. Epub 2021 Apr 30 doi: 10.1136/jclinpath-2021-207426. PMID: 33931563
Ahmad AJ, Parekh S, Ashley PF
Eur Arch Paediatr Dent 2018 Oct;19(5):311-320. Epub 2018 Sep 5 doi: 10.1007/s40368-018-0357-5. PMID: 30187262Free PMC Article
Whyte MP
Bone 2017 Sep;102:15-25. Epub 2017 Feb 24 doi: 10.1016/j.bone.2017.02.011. PMID: 28238808
Tonetti MS, Mombelli A
Ann Periodontol 1999 Dec;4(1):39-53. doi: 10.1902/annals.1999.4.1.39. PMID: 10863374

Diagnosis

Patel S, Saberi N, Pimental T, Teng PH
Int Endod J 2022 Oct;55 Suppl 4(Suppl 4):892-921. Epub 2022 Mar 30 doi: 10.1111/iej.13715. PMID: 35229320Free PMC Article
Fenn JS, Lorde N, Ward JM, Borovickova I
J Clin Pathol 2021 Oct;74(10):635-640. Epub 2021 Apr 30 doi: 10.1136/jclinpath-2021-207426. PMID: 33931563
Yates TM, Drucker M, Barnicoat A, Low K, Gerkes EH, Fry AE, Parker MJ, O'Driscoll M, Charles P, Cox H, Marey I, Keren B, Rinne T, McEntagart M, Ramachandran V, Drury S, Vansenne F, Sival DA, Herkert JC, Callewaert B, Tan WH, Balasubramanian M
Hum Mutat 2020 May;41(5):1042-1050. Epub 2020 Mar 5 doi: 10.1002/humu.24001. PMID: 32097528
Simon S, Resch H
Wien Med Wochenschr 2020 Apr;170(5-6):112-115. Epub 2020 Feb 18 doi: 10.1007/s10354-020-00736-3. PMID: 32072352
Mornet E
Orphanet J Rare Dis 2007 Oct 4;2:40. doi: 10.1186/1750-1172-2-40. PMID: 17916236Free PMC Article

Therapy

Dommisch H, Walter C, Difloe-Geisert JC, Gintaute A, Jepsen S, Zitzmann NU
J Clin Periodontol 2022 Jun;49 Suppl 24:149-166. Epub 2021 Dec 1 doi: 10.1111/jcpe.13563. PMID: 34854115
Fenn JS, Lorde N, Ward JM, Borovickova I
J Clin Pathol 2021 Oct;74(10):635-640. Epub 2021 Apr 30 doi: 10.1136/jclinpath-2021-207426. PMID: 33931563
Afanasyev DE, Liubarets SF
Probl Radiac Med Radiobiol 2020 Dec;25:18-55. doi: 10.33145/2304-8336-2020-25-18-55. PMID: 33361828
Bhujel N, Duggal MS, Saini P, Day PF
Eur Arch Paediatr Dent 2016 Dec;17(6):423-434. Epub 2016 Nov 3 doi: 10.1007/s40368-016-0247-7. PMID: 27812892
Straka M, Straka-Trapezanlidis M, Deglovic J, Varga I
Neuro Endocrinol Lett 2015;36(5):401-6. PMID: 26707036

Prognosis

Fenn JS, Lorde N, Ward JM, Borovickova I
J Clin Pathol 2021 Oct;74(10):635-640. Epub 2021 Apr 30 doi: 10.1136/jclinpath-2021-207426. PMID: 33931563
Yates TM, Drucker M, Barnicoat A, Low K, Gerkes EH, Fry AE, Parker MJ, O'Driscoll M, Charles P, Cox H, Marey I, Keren B, Rinne T, McEntagart M, Ramachandran V, Drury S, Vansenne F, Sival DA, Herkert JC, Callewaert B, Tan WH, Balasubramanian M
Hum Mutat 2020 May;41(5):1042-1050. Epub 2020 Mar 5 doi: 10.1002/humu.24001. PMID: 32097528
Whyte MP
Bone 2017 Sep;102:15-25. Epub 2017 Feb 24 doi: 10.1016/j.bone.2017.02.011. PMID: 28238808
Holan G, Needleman HL
Dent Traumatol 2014 Apr;30(2):100-6. Epub 2013 Oct 20 doi: 10.1111/edt.12081. PMID: 24138100
Mornet E
Orphanet J Rare Dis 2007 Oct 4;2:40. doi: 10.1186/1750-1172-2-40. PMID: 17916236Free PMC Article

Clinical prediction guides

Pierpont EI, Simmons JH, Spurlock KJ, Shanley R, Sarafoglou KM
Orphanet J Rare Dis 2021 Feb 12;16(1):80. doi: 10.1186/s13023-021-01722-7. PMID: 33579333Free PMC Article
Nadelman P, Bedran N, Magno MB, Masterson D, de Castro ACR, Maia LC
Int J Paediatr Dent 2020 Nov;30(6):687-712. Epub 2020 Apr 20 doi: 10.1111/ipd.12644. PMID: 32243000
Yates TM, Drucker M, Barnicoat A, Low K, Gerkes EH, Fry AE, Parker MJ, O'Driscoll M, Charles P, Cox H, Marey I, Keren B, Rinne T, McEntagart M, Ramachandran V, Drury S, Vansenne F, Sival DA, Herkert JC, Callewaert B, Tan WH, Balasubramanian M
Hum Mutat 2020 May;41(5):1042-1050. Epub 2020 Mar 5 doi: 10.1002/humu.24001. PMID: 32097528
Khan AA, Josse R, Kannu P, Villeneuve J, Paul T, Van Uum S, Greenberg CR
Osteoporos Int 2019 Sep;30(9):1713-1722. Epub 2019 Mar 26 doi: 10.1007/s00198-019-04921-y. PMID: 30915507
Tonetti MS, Mombelli A
Ann Periodontol 1999 Dec;4(1):39-53. doi: 10.1902/annals.1999.4.1.39. PMID: 10863374

Recent systematic reviews

Dommisch H, Walter C, Difloe-Geisert JC, Gintaute A, Jepsen S, Zitzmann NU
J Clin Periodontol 2022 Jun;49 Suppl 24:149-166. Epub 2021 Dec 1 doi: 10.1111/jcpe.13563. PMID: 34854115
Nadelman P, Bedran N, Magno MB, Masterson D, de Castro ACR, Maia LC
Int J Paediatr Dent 2020 Nov;30(6):687-712. Epub 2020 Apr 20 doi: 10.1111/ipd.12644. PMID: 32243000
Wagle M, D'Antonio F, Reierth E, Basnet P, Trovik TA, Orsini G, Manzoli L, Acharya G
BMJ Open 2018 Mar 2;8(3):e018556. doi: 10.1136/bmjopen-2017-018556. PMID: 29500202Free PMC Article
Bhujel N, Duggal MS, Saini P, Day PF
Eur Arch Paediatr Dent 2016 Dec;17(6):423-434. Epub 2016 Nov 3 doi: 10.1007/s40368-016-0247-7. PMID: 27812892
Tunison W, Flores-Mir C, ElBadrawy H, Nassar U, El-Bialy T
Pediatr Dent 2008 Jul-Aug;30(4):297-302. PMID: 18767508

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