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Hypodontia is defined as the developmental absence of one or more teeth excluding the third molars. It is one of the most common dental anomalies, and can have a negative impact on function, and also appearance. It rarely occurs in primary teeth (also known as deciduous, milk, first and baby teeth) and the most commonly affected are the adult second premolars and the upper lateral incisors. It usually occurs as part of a syndrome that involves other abnormalities and requires multidisciplinary treatment.

The phenomenon can be subdivided into the following according to the number of teeth concerned:

1. Hypodontia: one to six missing teeth excluding the third molars
2. Oligodontia: six or more missing permanent teeth excluding the third molars
3. Anodontia: complete absence of teeth

Signs and symptoms

Typically, all baby teeth will be present by the age of three. As for all adult teeth, they erupt between the ages 6 to 14, with the exception of the third molar, also known as the wisdom teeth which normally erupt between 17 and 25 years of age. If the tooth has yet to erupt by an appropriate age, panoramic x-rays are taken.

Dental features

Microdontia may be present in one or more of the other teeth. This means that the teeth appear smaller than normal, may be observed in both the primary and permanent dentition. This condition can be genetically-linked and in severe cases, may present themselves in the form of ectodermal dysplasia, cleft lip or palate or Down Syndrome. A delay in tooth development may also serve as an indication, whereby the absence of an adult successor slows down the normal resorption of the roots of the baby teeth, which is the progressive loss of parts of the tooth.

Misplaced (ectopic) positioning of the adult teeth may be discovered upon examination or a radiograph. One of the consequences may be an adult tooth intercepting with a baby tooth, causing premature loss or wrong positioning. This can be due to either the absence of neighboring teeth acting as a guide during eruption or the lack of space in the jaw for them to erupt into because of malocclusion.

Skeletal features

Several studies have discovered that anteriorly missing teeth can accompany retrognathic maxilla, also known as an underbite, prognathic mandible, where the lower jaw protrudes out more than normal, and smaller posterior cranial base length. Occurrence of hypodontia can be associated with reduced anterior lower facial height and lip protrusion. This can be linked to lower maxillary to mandibular plane angles.

A more acute mandibular angle and flatter chin may develop as a result. These characteristics become more prominent as the condition becomes progressively severe, particularly when more than one tooth is missing.

Other dental and radiographic features

Data derived from principal component analysis of radiographic images show that children with mild hypodontia may display significant increase of the interincisal angle and decrease in the maxillary and mandibular incisor angles.

Cephalometric tracing is commonly used to study a patient's dentofacial proportions in the craniofacial complex. This can aid in predicting growth changes, allowing dentists, especially orthodontists, to develop a suitable treatment plan. Coupled with that, findings consistent among individuals include:

1. Anterior hypodontia associated with hyper divergent craniofacial pattern;
2. A tendency toward a class III malocclusion identified in maxillary hypodontia, and;
3. Reduced lower posterior facial height in children with posterior and mandibular hypodontia.

Associated anomalies

1. Reduction in coronal or radical dimensions
2. Retained primary teeth
3. Ectopic canine eruption
4. Abnormal morphology such as peg-shaped maxillary lateral incisors and taurodontism, characterized by an enlarged tooth body and roots that are reduced in size
5. Extracted teeth

Cause

Several theories regarding the aetiology of hypodontia have been proposed in existing literature. There have been various theories mostly looking into genetic and environmental aspects and how they may both be involved. However, the exact cause remains unclear. The extent of individual influences of genetic and environmental factors is still widely debated.

Theories regarding the mechanism through which hypodontia occurs can be categorised into evolutional or anatomical.

Preliminary studies focused on an evolutionary approach which suggested shortening of the intermaxillary complex and thus shorter arches may contribute to a decrease in number of teeth. This was also suggested in 1945 by Dahlberg using Butler's Field Theory that focused on evolution and development of mammalian teeth into human dentition in an attempt to analyse different of agenesis. In each jaw, four morphological sites were identified (incisors, canines, premolars and molars). The tooth at the end of each region was less genetically stable and hence more prone to absence. In contrast, the tooth most mesial in each region seemed to be more genetically stable. A subsequent theory hypothesised the teeth at the end of each region were possibly "vestigial bodies" that became obsolete during the evolutionary process. At present, it has been theorised that evolutionary change is working to decrease the human dentition by the loss of an incisor, premolar and molar in each quadrant. According to Vastardis (2000), the size of jaws and number of teeth seem to decrease along with human evolution.

Theories focusing on anatomical principle, hypothesised that specific areas of the dental lamina are especially prone to environmental effects during tooth maturation. Svinhufvud et al. (1988) suggested that teeth that were more prone to absence developed in areas of initial fusion of the jaw. For instance, maxillary lateral incisors originate where the lateral maxillae and medial nasal bone processes fuse. In contrast, Kjaer et al. (1994) suggested regions where innervation developed were more sensitive than areas of fusion. Commonly affected regions were found to undergo innervation last, this might imply the developmental relationship between nerve and hard tissue. It is thought to be local nerve development that affects tooth agenesis rather than global development, as brainstem anomalies have not been seen to affect tooth development.

Presently, the role of polygenic and environmental factors on hypodontia is recognised in most theories.

Environmental factors

Environmental factors can be classified into two main groups, invasive and non-invasive. These factors act additively or independently, ultimately affecting positioning and physical development of the tooth.

Invasive environmental factors potentially affect tooth development and positioning leading to hypodontia and impaction. Examples include jaw fractures, surgical procedures and extraction of the preceding deciduous tooth. Treatment such as irradiation has been shown to have severe effects on developing teeth. In a smaller capacity, chemotherapy was also found to have a similar effect. Thalidomide (N-phthaloylglutamine) was also discovered to have a causative effect on mothers who took the drug during pregnancy, resulting in congenitally missing teeth in their children. A link was found between systemic diseases, endocrine disruption (i.e. idiopathic hypoparathyroidism and pseudohypoparathyroidism) and ectodermal dysplasia. However, a definite etiological relationship has yet to be established. Examples of infections include rubella and candida. Exposure to PCBs (such as dioxin), allergies, and toxic epidermal necrolysis following a drug reaction may also be contributing factors.

In a recent study assessing environmental risk factors for hypodontia, it was established that maternal smoking does play a causative role in hypodontia. Passive smoking and caffeine were also assessed but showed no statistical significance.

The Journal of the American Dental Association published preliminary data suggesting a statistical association between hypodontia of the permanent teeth and epithelial ovarian cancer (EOC). The study shows that women with EOC are 8.1 times more likely to have hypodontia than are women without EOC. The suggestion therefore is that hypodontia can serve as a "marker" for potential risk of EOC in women.

Genetics

Genetic causes also involve the genes MSX1 and PAX9.

Genetic associations for selective tooth agenesis ("STHAG") include:

Failure of tooth formation due to disturbances during the early stages of development could be the cause of congenital missing teeth; this is also known as tooth agenesis. A variety of studies show that missing teeth are commonly associated with genetic and environmental factors. Some literature also shows that a combination of both factors may contribute to the occurrence of hypodontia.

Most craniofacial characteristics are influenced by both genetic and environmental factors through complex interactions. The variable expressivity of traits can be either completely genetically determined, environmentally determined, or both. That genetics plays an important role in hypodontia is shown in many different cases. There are hundreds of genes expressed and involved in regulating tooth morphogenesis. Although a single gene defect may contribute to hypodontia, more studies propose that hypodontia is the result of one or more points of closely linked genetic mutations, or polygenic defects.

The pattern of congenitally missing teeth seen in monozygotic twins is different, suggesting an underlying epigenetic factor, which may be due to the simultaneous occurrence of two anomalies. This multifactorial aetiology involves environmental factors which trigger the genetic anomalies, resulting in the occurrence of dental agenesis. Common environmental factors include infection, trauma and drugs which predispose to the condition. In hereditary cases, evidence of dental germ developing after surrounding tissues have closed the space required for development may be a large contributing factor, as well as such genetic disorders as Down syndrome, ectodermal dysplasia, cleidocranial dysplasia, and cleft lip and cleft palate.

MSX1

MSX1 (muscle segment homeobox 1) is involved in condensation of ectomesenchyme in the tooth germ. Among the members of homeobox genes, MSX1 and MSX2 are crucial in mediating direct epithelial-mesenchymal interactions during tooth development by expressing in regions of condensing ectomesenchyme in the tooth germ. MSX1 mutations have been identified as a contributing factor in missing second premolars, third molars, and a small percentage of first molars. MSX1 is less likely to cause anterior agenesis.

Heterozygous mutations in PAX9 (paired box gene 9) could arrest tooth morphogenesis as it plays a role of transcription the gene expressed in tooth mesenchyme at the bud stage during tooth development. A study showed that single nucleotide polymorphisms in PAX9 were highly associated with missing upper lateral incisors.

AXIN2

The AXIN2 (AXIS inhibition protein 2) gene is a negative regulator of the Wnt signalling pathway, which is important in regulating cell fate, proliferation, differentiation and apoptosis. Its polymorphic variant may be associated with hypodontia such as missing lower incisors or in a more severe form of agenesis like oligontia (lack of six or more permanent teeth).

EDA

EDA provides instructions for making a protein called ectodysplasin A. It encodes transmembrane protein that is part of TNF (tumour necrosis factor) family of ligands. EDA gene defects cause ectodermal dysplasia, which is also known as X-linked hypohidrotic ectodermal dysplasia. Common dental features of ectodermal dysplasia are multiple missing teeth and microdontia.

PAX9 and TGFA are involved in regulating between MSX1 and PAX9, causing hypodontia of the molars.

Hypodontia can be found in isolated cases too. The familiar or sporadic type of isolations are more frequently reported than the syndromic type. Isolated cases of autosomal dominant, autosomal recessive, or X-linked inheritance patterns may have an impact on the isolation conditions in expressing variation of both penetration and expressivity of traits. Mutations in MSX, PAX9 and TGFA genes are known to cause congenitally missing teeth in some racial groups.

Research

In the 1960s and 1970s, several studies were conducted sponsored by the U.S. Atomic Energy Commission, with the aim of finding a link between genetics and hypodontia.

Impact

There are numerous studies and research reports on the prevalence, aetiology, and treatment of hypodontia and the dentoskeletal effect of hypodontia. A few studies have investigated Oral Health-related Quality of Life (OHRQoL) in individuals with hypodontia and provided some evidence that hypodontia may have an impact on quality of life.

Psychosocial

Cosmetic dentistry has become more notable and prevalent in modern society. Interpersonal relationships and perceived qualities, such as intelligence, friendliness, social class, and popularity can be affected by dentofacial appearance. Some studies have shown that the extent of complaints made by patients was associated with the severity of the condition and the number of missing permanent teeth.

Meta-analyses and theoretical reviews have demonstrated that attractive children are seen by others as more intelligent and exhibit more positive social behaviour and traits, other than receiving much more positive treatment than their less attractive counterparts. Therefore, a divergence from perceived ideal dentofacial aesthetic, particularly in children, might adversely affect self-esteem and self-confidence besides attracting mockery from peers.

It is therefore reasonable to theorize that deviations from "normal" or "ideal" dentofacial aesthetic could be destructive to an individual's psychosocial and emotional well-being, which brings upon some psychosocial distress in that individual as a result of their condition.

Functional

Individuals with hypodontia tend to have deeper bites and spaces. Further deepening of the bite can also be seen on individuals with missing posterior teeth. Apart from that, hypodontia may lead to non-working interferences, poor gingival contours and over-eruptions of the opposing teeth.

It has been found that individuals with hypodontia experience more difficulty during mastication or functioning movements due to smaller occlusal table available. A recent cross-sectional study showed that hypodontia patients have more difficulties in chewing, especially if the deciduous teeth associated with the missing permanent teeth had been exfoliated. Despite currently limited evidence to support this statement, it is plausible that hypodontia may pose functional limitations, which eventually affect that individual's general well-being and quality of life.

Hypodontia can indeed pose limitations on the chewing ability of a patient. The condition can be associated with split in the upper lips – a condition known as oral cleft. Hypodontia can have impacts on speech, aesthetics and function of muscles in the mouth. As a result, hypodontia can have negative impacts on the quality of life, although the condition can be well managed and treated by dentists and orthodontists. To manage the condition, the patient will need to have long-term orthodontic treatment.

Financial

Patient with hypodontia requires careful treatment plan due to complex case in order to ensure the best treatment outcomes. Such treatment plans require multi-disciplinary approach, which usually come at a financial cost to both patient and possibly their family. Due to this reason, a team consists of different dental specialties is involved in the patient care.

Management

Hypodontia is a condition that can present in various ways with differing severities. This results in a wide range of treatment methods available. Those affected should be allowed to consider and select the most suitable option for themselves. Early diagnosis of hypodontia is critical for treatment success. The treatment of hypodontia involves specialists in departments such as oral and maxillofacial surgery, operative dentistry, pediatric dentistry, orthodontics and prosthodontics.

Before determining a treatment plan, the following should be determined:

• Evaluate the number of teeth missing
• The size and number of remaining teeth in both arches
• Malocclusion
• Facial profile
• Bone volume
• Age: Definitive treatment for hypodontia only commences once all permanent teeth erupt, or upon the completion of orthodontic treatment
• Primary teeth condition
• Patient's motivation towards treatment

Traditionally, the management of hypodontia has involved replacing missing teeth. By replacing the missing teeth, it can prevent neighbouring teeth tilting or drifting and also prevents the overeruption of opposing teeth which could then impact on occlusion and temporo-mandibular joint dysfunction and impact the patient's susceptibility to gum disease, tooth wear and tooth fractures. However, studies have suggested that a stable occlusion can be achieved even with a shortened arch of 10 occluding pairs of teeth. The findings support the concept that a healthy and stable occlusion can exist despite missing teeth as long as an acceptable number of teeth are in occlusion. However, this management technique may not be suitable for those with gum disease, parafunctioning activity (tooth grinding or clenching) or malocclusion.

It should also be noted that spaces within the dental arch should be monitored, especially in younger patients, as teeth are more likely to drift, tilt or over-erupt. To do this, study models and clinical photographs could be taken in order to record baseline records. If tooth movement was to occur, another form of management may be required depending on the severity and nature.

The following below are the methods used to manage hypodontia:

Accept spacing

This is a method suitable to individuals if the space from a missing tooth is not deemed to be an aesthetic concern. Appearance may not be a problem in some cases, for example, when spacing present behind the canines may not be particularly visible, depending on the individual.

Management of retained primary teeth

When there is a case of hypodontia of the permanent premolar teeth, the primary molar teeth would often remain in the mouth beyond the time they are meant to be lost. Therefore, with a presence of healthy primary teeth in the absence of a permanent successor, retaining the primary teeth can be a feasible management of hypodontia.

The primary molars present also functions as a space maintainer, prevent alveolar bone resorption and delays future prosthodontic space replacement by acting as a semi permanent solution going into adulthood Previous studies also shown a good prognosis of retained primary molars going into adulthood. However, leaving the primary teeth in place may run the risk of tooth infraocclusion where the occlusal surface is below that of adjacent teeth.

Despite this, the retention of primary teeth, particularly molars, are more susceptible to occlusal wear, over-eruption of opposing teeth and the loss of inter-occlusal space.

Orthodontic space closure

Orthodontic space closure is a way of using orthodontics in order to close spaces in the mouth where the teeth are missing. The ideal age for definitive orthodontic treatment is early adolescence but it is important to consider the patient's age, severity of hypodontia, patient expectations and their commitment to treatment. It can be an option for hypodontia management in the case of missing maxillary lateral incisors through the reshaping, and mesial re-positioning of the adjacent canine. This management is indicated in hypodontia cases of Class I molar relationship with severe crowding in the mandibular anterior region where the extraction of lower premolar leads to a predictable outcome, and Class II molar relationship in the absence of crowding and protrusion of the mandibular anterior dentition.

When moving the canine into the space of the lateral incisor, the dimensions of the canine, root position and gingival position differ from a lateral incisor and therefore preparation of the canine is necessary in order for it to mimic the incisor. This may involve:

• Reduction of the incisal tip and addition of composite on the incisal edge to create a straight contour and a rounded disto-incisal corner
• Reduction of the mesial and distal surfaces to reduce the width of the tooth
• Flattening of the labial surface to reduce bulbosity. However, removal of enamel by expose the darker coloured dentine and therefore further restoration may be required.
• Preparation of the palatal surface of the canine to reduce its bulk.

The use of veneers can also be used instead of composite however, these are more expensive and more time-consuming.

There have been several studies which showed the advantages of orthodontic space closure without prosthodontic space replacements. The main advantage mentioned is the early completion of the treatment during early adolescence and the long lasting result of the treatment outcome. In individuals with a high smile line, the mesial re-positioning of canine maintains the normal soft tissue architecture is important in maintaining the aesthetic appearance. This option also negates the risks and costs that comes with prosthodontic treatment and the impression that there is no missing tooth.

Some factors need to be considered when making a decision whether to undergo space closure. These include facial profile, size and dimension of canine, the shade of colour of the teeth and the gingival contour and height. Group function occlusion is usually present as a result of the mesial movement of the canine. In order to maintain the stability of the closed space, direct-bonded lingual retainers are usually required.

Orthodontic space opening prior to prosthodontic treatment

The need for orthodontic space opening prior to prosthodontic management depends on the amount of edentulous space available in relation to adjacent teeth, occlusion and aesthetic concerns. To determine the amount of space needed, three methods in the literature can be used which are the golden proportion, the Bolton Analysis and comparing the edentulous space with the contralateral tooth size if present.

Space opening and prosthodontic treatment is indicated where there is a Class I molar relationships in the absence of malocclusion Class III molar relationships presenting with a concave facial profile. However, the alteration in appearance during orthodontic treatment (e.g. creating diastema for placement of prostheses) before the filling up the space, although temporary, can negatively impact the oral health-related quality of life in adolescents.

Removable partial dentures

Removable partial dentures are known to be an effective interim method for maintaining functional and aesthetic demands in a growing patient, where definitive fixed restorations are not suitable yet. Removable dentures act as a space maintainer and also prevent the migration of adjacent or opposing teeth, thereby preserving the face height. They are also easy to adjust or add on to in the event of further tooth eruption. However, it may be difficult for young individuals to adhere with wearing removable dentures, due to their bulk. Some patients also find the idea of dentures functionally and socially unacceptable, making them unwilling to comply. Removable prosthetic devices are also known to cause damage to the remaining teeth if worn over a long period of time.

Conventional crown and bridgework

Fixed restorative options are generally preferred over removable ones.

• Resin-bonded bridges: Due to its minimal preparation required, this method of replacing teeth is more suited to young adults. It is a definitive restoration with the ability to fill up one or two tooth spaces. Research has reflected a survival rate of 80% over a period of 6 years or longer, and that cantilever resin-bonded bridges are at least as good as conventional fixed-fixed bridges. Restoring teeth with this method can only be done after orthodontic treatment and will need an element of retention to ensure that tooth contacts are not misplaced.
• Conventional bridges: Teeth tend to be prepared for conventional bridgework if there are large restorations present, thus being more commonly done on adult patients with hypodontia. Treatment with conventional bridgework will require significant reduction of tooth structure, which will put the tooth at risk of biological damage i.e. loss of vitality. This risk is especially high in young patients with large pulp chambers.

Tooth autotransplantation

Autotransplantation involves the removal of a tooth from one socket and relocating to another socket in the same individual. If done successfully, it is able to ensure stable alveolar bone volume as there is continuous stimulation of the periodontal ligament.

Implant supported tooth replacement

Placing dental implants has proven to be a predictable and reliable method of treating hypodontia, along with bringing excellent aesthetic results. Implant placement should be delayed until jaw growth in an individual is complete. One limitation of implant placement would be the need for a sufficient amount of bone volume, which if not met, may affect the positioning of the implant. However, bone grafting can be carried out to overcome this.

Epidemiology

Hypodontia is less common in the primary dentition, with reported prevalence rates ranging from 0.5% in the Icelandic population to 2.4% in the Japanese population. In the primary dentition the teeth reported as most likely to be missing are the lateral incisors, both maxillary and mandibular. If a deciduous tooth is missing this will increase the risk of an absent successor.

In the permanent dentition third molars are most commonly absent, and one study found prevalence rates of between 20–22%. When third molars are ignored the prevalence rate for each tooth varies from study to study. In Caucasian studies mandibular second premolars and maxillary lateral incisors are most often absent. Several UK studies have found the lower second premolar to be most commonly absent. Studies from Asian populations report that the mandibular incisor is most commonly absent.

A higher prevalence of hypodontia in females has been reported. The most extensive studies have been in Caucasian populations and suggest a prevalence of 4–6%.

One study looked at 33 previous studies with a sample size of 127,000, and concluded that the prevalence of hypodontia in the permanent dentition varied between continents, racial groups and genders. In the white European population they suggested a prevalence of 4.6% in males and 6.3% in females. In an African-American sample they found this to be 3.2% in males and 4.6% in females. The same study found that in the permanent dentition the most likely teeth to be missing and the frequency of these missing teeth was:

• Mandibular second premolar 3%
• Maxillary lateral incisor 1.7%
• Maxillary second premolar 1.5%
• Mandibular central incisor 0.3%

References

1. ^ Mestrović SR, Rajić Z, Papić JS (December 1998). "Hypodontia in patients with Down's syndrome". Collegium Antropologicum. 22 Suppl: 69–72. PMID 9951143.
2. Rakhshan, Vahid (2015). "Congenitally missing teeth (hypodontia): A review of the literature concerning the etiology, prevalence, risk factors, patterns and treatment". Dental Research Journal. 12 (1): 1–13. doi:10.4103/1735-3327.150286. ISSN 1735-3327. PMC 4336964. PMID 25709668.
3. ^ Batwa, Waeil; Almarhoon, Hala A; Almoammar, Khalid A; Alqahtani, Nasser; Albarakati, Sahar F; Al-Jewair, Thikriat (2018-11-08). "Dento-skeletal characteristics of cleft patients with missing teeth". Clinical, Cosmetic and Investigational Dentistry. 10: 237–244. doi:10.2147/CCIDE.S170717. ISSN 1179-1357. PMC 6233474. PMID 30519115.
4. Jayashankara, CM; Shivanna, Anil Kumar; Sridhara, KS; Kumar, Paluvary Sharath (2013). "Taurodontism: A dental rarity". Journal of Oral and Maxillofacial Pathology. 17 (3): 478. doi:10.4103/0973-029X.125227. ISSN 0973-029X. PMC 3927363. PMID 24574680.
5. Al-Ani AH, Antoun JS, Thomson WM, Merriman TR, Farella M (2017). "Hypodontia: An Update on Its Etiology, Classification, and Clinical Management". BioMed Research International. 2017: 9378325. doi:10.1155/2017/9378325. PMC 5376450. PMID 28401166.
6. ^ Larmour CJ, Mossey PA, Thind BS, Forgie AH, Stirrups DR (April 2005). "Hypodontia--a retrospective review of prevalence and etiology. Part I". Quintessence International. 36 (4): 263–70. PMID 15835422.
7. ^ Galluccio G, Castellano M, La Monaca C (July 2012). "Genetic basis of non-syndromic anomalies of human tooth number". Archives of Oral Biology. 57 (7): 918–30. doi:10.1016/j.archoralbio.2012.01.005. PMID 22325622.
8. Husam, Al-Ani, Azza (2016). Genetic and environmental factors associated with hypodontia (Thesis). University of Otago. hdl:10523/6866.{{cite thesis}}: CS1 maint: multiple names: authors list (link)
9. Hobkirk JA, Goodman JR, Jones SP (November 1994). "Presenting complaints and findings in a group of patients attending a hypodontia clinic". British Dental Journal. 177 (9): 337–9. doi:10.1038/sj.bdj.4808606. PMID 7980981. S2CID 13294116.
10. Vastardis H (June 2000). "The genetics of human tooth agenesis: new discoveries for understanding dental anomalies". American Journal of Orthodontics and Dentofacial Orthopedics. 117 (6): 650–6. doi:10.1016/s0889-5406(00)70173-9. PMID 10842107. S2CID 11886845.
11. Svinhufvud E, Myllärniemi S, Norio R (December 1988). "Dominant inheritance of tooth malpositions and their association to hypodontia". Clinical Genetics. 34 (6): 373–81. doi:10.1111/j.1399-0004.1988.tb02895.x. PMID 3233785. S2CID 30376609.
12. ^ Kjaer I, Kocsis G, Nodal M, Christensen LR (October 1994). "Aetiological aspects of mandibular tooth agenesis—focusing on the role of nerve, oral mucosa, and supporting tissues". European Journal of Orthodontics. 16 (5): 371–5. doi:10.1093/ejo/16.5.371. PMID 7805810.
13. ^ J Pemberton T, Das P, Patel P (2004-11-30). "Hypodontia: Genetics and future perspectives". Brazilian Journal of Oral Sciences. 4 (13).
14. Sutphin A, Albright F, McCune DJ (1943). "Five cases (3 in siblings) of idiopathic hypoparathyroidism associated with moniliasis". J. Clin. Endocrinol. 3 (12): 625–634. doi:10.1210/jcem-3-12-625.
15. Wu CC, Wong RW, Hägg U (2007). "A review of hypodontia: the possible etiologies and orthodontic, surgical and restorative treatment options—conventional and futuristic" (PDF). Hong Kong Dental Journal. 4: 113–21.
16. Kinirons MJ (June 1983). "Candidal invasion of dentine complicating hypodontia". British Dental Journal. 154 (12): 400–1. doi:10.1038/sj.bdj.4805102. PMID 6576802. S2CID 19669502.
17. Alaluusua S, Lukinmaa PL, Torppa J, Tuomisto J, Vartiainen T (January 1999). "Developing teeth as biomarker of dioxin exposure". Lancet. 353 (9148): 206. doi:10.1016/S0140-6736(05)77214-7. PMID 9923879. S2CID 31562457.
18. Alaluusua S, Calderara P, Gerthoux PM, Lukinmaa PL, Kovero O, Needham L, Patterson DG, Tuomisto J, Mocarelli P (September 2004). "Developmental dental aberrations after the dioxin accident in Seveso". Environmental Health Perspectives. 112 (13): 1313–8. doi:10.1289/ehp.6920. PMC 1247522. PMID 15345345.
19. Guo YL, Lambert GH, Hsu CC, Hsu MM (April 2004). "Yucheng: health effects of prenatal exposure to polychlorinated biphenyls and dibenzofurans". International Archives of Occupational and Environmental Health. 77 (3): 153–8. doi:10.1007/s00420-003-0487-9. PMID 14963712. S2CID 21321352.
20. Yamaguchi T, Tomoyasu Y, Nakadate T, Oguchi K, Maki K (December 2008). "Allergy as a possible predisposing factor for hypodontia". European Journal of Orthodontics. 30 (6): 641–4. doi:10.1093/ejo/cjn043. PMID 18687988.
21. Gaultier F, Rochefort J, Landru MM, Allanore L, Naveau A, Roujeau JC, Gogly B (November 2009). "Severe and unrecognized dental abnormalities after drug-induced epidermal necrolysis". Archives of Dermatology. 145 (11): 1332–3. doi:10.1001/archdermatol.2009.233. PMID 19917972.
22. Al-Ani AH, Antoun JS, Thomson WM (August 2017). "Maternal Smoking During Pregnancy is associated with Offspring Hypodontia". J Dent Res. 96 (9): 1014–1019. doi:10.1177/0022034517711156. PMID 28535361. S2CID 11423326.
23. Chalothorn LA, Beeman CS, Ebersole JL, Kluemper GT, Hicks EP, Kryscio RJ, DeSimone CP, Modesitt SC (February 2008). "Hypodontia as a risk marker for epithelial ovarian cancer: a case-controlled study". Journal of the American Dental Association. 139 (2): 163–9. doi:10.14219/jada.archive.2008.0132. PMID 18245684.
24. Nieminen P (June 2009). "Genetic basis of tooth agenesis". Journal of Experimental Zoology Part B: Molecular and Developmental Evolution. 312B (4): 320–42. doi:10.1002/jez.b.21277. PMID 19219933.
25. De Coster PJ, Marks LA, Martens LC, Huysseune A (January 2009). "Dental agenesis: genetic and clinical perspectives". Journal of Oral Pathology & Medicine. 38 (1): 1–17. doi:10.1111/j.1600-0714.2008.00699.x. PMID 18771513.
26. Harris EF (June 2008). "Interpreting heritability estimates in the orthodontic literature". Seminars in Orthodontics. 14 (2): 125–134. doi:10.1053/j.sodo.2008.02.003.
27. Bäckman B, Wahlin YB (January 2001). "Variations in number and morphology of permanent teeth in 7-year-old Swedish children". International Journal of Paediatric Dentistry. 11 (1): 11–7. doi:10.1046/j.1365-263x.2001.00205.x. PMID 11309867.
28. Kapadia H, Mues G, D'Souza R (August 2007). "Genes affecting tooth morphogenesis". Orthodontics & Craniofacial Research. 10 (3): 105–13. doi:10.1111/j.1601-6343.2007.00395.x. PMID 17651126.
29. ^ Alves-Ferreira M, Pinho T, Sousa A, Sequeiros J, Lemos C, Alonso I (May 2014). "Identification of genetic risk factors for maxillary lateral incisor agenesis". Journal of Dental Research. 93 (5): 452–8. doi:10.1177/0022034514523986. PMID 24554542. S2CID 20561426.
30. Vastardis H (June 2000). "The genetics of human tooth agenesis: new discoveries for understanding dental anomalies". American Journal of Orthodontics and Dentofacial Orthopedics. 117 (6): 650–6. doi:10.1016/S0889-5406(00)70173-9. PMID 10842107. S2CID 11886845.
31. "Hypodontia—a Retrospective Review of Prevalence and Etiology. Part I". Retrieved 2018-10-22.
32. Brook AH (1984-01-01). "A unifying aetiological explanation for anomalies of human tooth number and size". Archives of Oral Biology. 29 (5): 373–8. doi:10.1016/0003-9969(84)90163-8. PMID 6611147.
33. ^ Rakhshan V (2015). "Congenitally missing teeth (hypodontia): A review of the literature concerning the etiology, prevalence, risk factors, patterns and treatment". Dental Research Journal. 12 (1): 1–13. doi:10.4103/1735-3327.150286. PMC 4336964. PMID 25709668.
34. "Ectodermal dysplasia and hypodontia". British Dental Journal. 212 (11): 523. June 2012. doi:10.1038/sj.bdj.2012.481.
35. Chopra R, Marwaha M, Chaudhuri P, Bansal K, Chopra S (2012). "Hypodontia and delayed dentition as the primary manifestation of cleidocranial dysplasia presenting with a diagnostic dilemma". Case Reports in Dentistry. 2012: 262043. doi:10.1155/2012/262043. PMC 3540686. PMID 23320199.
36. Slayton RL, Williams L, Murray JC, Wheeler JJ, Lidral AC, Nishimura CJ (May 2003). "Genetic association studies of cleft lip and/or palate with hypodontia outside the cleft region". The Cleft Palate-Craniofacial Journal. 40 (3): 274–9. doi:10.1597/1545-1569_2003_040_0274_gasocl_2.0.co_2. PMC 2752356. PMID 12733956.
37. ^ MacKenzie A, Ferguson MW, Sharpe PT (June 1992). "Expression patterns of the homeobox gene, Hox-8, in the mouse embryo suggest a role in specifying tooth initiation and shape". Development. 115 (2): 403–20. doi:10.1242/dev.115.2.403. PMID 1358591.
38. Gökkaya B, Motro M, Kargül B (2015). "Prevalence and characteristics of non-syndromic hypodontia among Turkish orthodontic patient population". Journal of International Society of Preventive & Community Dentistry. 5 (3): 170–5. doi:10.4103/2231-0762.159952. PMC 4515798. PMID 26236675.
39. Vastardis H, Karimbux N, Guthua SW, Seidman JG, Seidman CE (August 1996). "A human MSX1 homeodomain missense mutation causes selective tooth agenesis". Nature Genetics. 13 (4): 417–21. doi:10.1038/ng0896-417. PMID 8696335. S2CID 731661.
40. Mitsui SN, Yasue A, Masuda K, Watanabe K, Horiuchi S, Imoto I, Tanaka E (March 2014). "Novel PAX9 mutations cause non-syndromic tooth agenesis". Journal of Dental Research. 93 (3): 245–9. doi:10.1177/0022034513519801. PMID 24436340. S2CID 1343341.
41. Cobourne MT, Sharpe PT (2012-05-25). "Diseases of the tooth: the genetic and molecular basis of inherited anomalies affecting the dentition". Wiley Interdisciplinary Reviews: Developmental Biology. 2 (2): 183–212. doi:10.1002/wdev.66. PMID 24009033. S2CID 25468458.
42. Callahan N, Modesto A, Meira R, Seymen F, Patir A, Vieira AR (January 2009). "Axis inhibition protein 2 (AXIN2) polymorphisms and tooth agenesis". Archives of Oral Biology. 54 (1): 45–9. doi:10.1016/j.archoralbio.2008.08.002. PMC 2643013. PMID 18790474.
43. Lammi L, Arte S, Somer M, Jarvinen H, Lahermo P, Thesleff I, Pirinen S, Nieminen P (May 2004). "Mutations in AXIN2 cause familial tooth agenesis and predispose to colorectal cancer". American Journal of Human Genetics. 74 (5): 1043–50. doi:10.1086/386293. PMC 1181967. PMID 15042511.
44. Mostowska A, Biedziak B, Jagodzinski PP (2006-01-24). "Axis inhibition protein 2 (AXIN2) polymorphisms may be a risk factor for selective tooth agenesis". Journal of Human Genetics. 51 (3): 262–6. doi:10.1007/s10038-005-0353-6. PMID 16432638.
45. "EDA ectodysplasin A [Homo sapiens (human)] - Gene - NCBI". ncbi.nlm.nih.gov. Retrieved 2018-10-22.
46. Kere J, Srivastava AK, Montonen O, Zonana J, Thomas N, Ferguson B, Munoz F, Morgan D, Clarke A, Baybayan P, Chen EY, Ezer S, Saarialho-Kere U, de la Chapelle A, Schlessinger D (August 1996). "X-linked anhidrotic (hypohidrotic) ectodermal dysplasia is caused by mutation in a novel transmembrane protein". Nature Genetics. 13 (4): 409–16. doi:10.1038/ng0895-409. PMID 8696334. S2CID 25690815.
47. "A Dentist Recognizes Ectodermal Dysplasia and Brings Welcome Relief to Family". Journal of the Canadian Dental Association. Retrieved 2018-10-22.
48. Arte S, Nieminen P, Apajalahti S, Haavikko K, Thesleff I, Pirinen S (May 2001). "Characteristics of incisor-premolar hypodontia in families". Journal of Dental Research. 80 (5): 1445–50. doi:10.1177/00220345010800051201. PMID 11437217. S2CID 30945991.
49. Goldenberg M, Das P, Messersmith M, Stockton DW, Patel PI, D'Souza RN (July 2000). "Clinical, radiographic, and genetic evaluation of a novel form of autosomal-dominant oligodontia". Journal of Dental Research. 79 (7): 1469–75. doi:10.1177/00220345000790070701. PMID 11005730. S2CID 8362122.
50. Pirinen S, Kentala A, Nieminen P, Varilo T, Thesleff I, Arte S (August 2001). "Recessively inherited lower incisor hypodontia". Journal of Medical Genetics. 38 (8): 551–6. doi:10.1136/jmg.38.8.551. PMC 1734917. PMID 11494968.
51. Ahmad W, Brancolini V, ul Faiyaz MF, Lam H, ul Haque S, Haider M, Maimon A, Aita VM, Owen J, Brown D, Zegarelli DJ, Ahmad M, Ott J, Christiano AM (April 1998). "A locus for autosomal recessive hypodontia with associated dental anomalies maps to chromosome 16q12.1". American Journal of Human Genetics. 62 (4): 987–91. doi:10.1086/301799. PMC 1377039. PMID 9529357.
52. Han D, Gong Y, Wu H, Zhang X, Yan M, Wang X, Qu H, Feng H, Song S (November 2008). "Novel EDA mutation resulting in X-linked non-syndromic hypodontia and the pattern of EDA-associated isolated tooth agenesis". European Journal of Medical Genetics. 51 (6): 536–46. doi:10.1016/j.ejmg.2008.06.002. PMID 18657636.
53. Graber LW (February 1978). "Congenital absence of teeth: a review with emphasis on inheritance patterns". Journal of the American Dental Association. 96 (2): 266–75. doi:10.14219/jada.archive.1978.0054. PMID 342579.
54. Niswander JD, Sujaku C (December 1963). "Congenital anomalies of teeth in Japanese children". American Journal of Physical Anthropology. 21 (4): 569–74. doi:10.1002/ajpa.1330210413. PMID 14185534.
55. Woolf CM (May 1971). "Missing maxillary lateral incisors: a genetic study". American Journal of Human Genetics. 23 (3): 289–96. PMC 1706719. PMID 5089845.
56. ^ Meaney, S.; Anweigi, L.; Ziada, H.; Allen, F. (2011-06-21). "The impact of hypodontia: a qualitative study on the experiences of patients". The European Journal of Orthodontics. 34 (5): 547–552. doi:10.1093/ejo/cjr061. ISSN 0141-5387. PMID 21693681.
57. ^ Emma, Laing (Jan 2010). "Psychosocial impact of hypodontia in children". American Journal of Orthodontics and Dentofacial Orthopedics. 137.
58. "PsycNET". psycnet.apa.org. Retrieved 2018-11-26.
59. Shaw, W C; O'Brien, K D; Richmond, S; Brook, P (1991). "Quality control in orthodontics: risk/benefit considerations". British Dental Journal. 170 (1): 33–37. doi:10.1038/sj.bdj.4807399. ISSN 0007-0610. PMID 2001299. S2CID 23761548.
60. SHEENA, KOTECHA. "The Impact of Hypodontia on the Oral Health Related-Quality of Life in Children" (PDF).
61. ^ Al-Ani, Azza Husam; Antoun, Joseph Safwat; Thomson, William Murray; Merriman, Tony Raymond; Farella, Mauro (2017). "Hypodontia: An Update on Its Etiology, Classification, and Clinical Management". BioMed Research International. 2017: 9378325. doi:10.1155/2017/9378325. ISSN 2314-6133. PMC 5376450. PMID 28401166.
62. Borzabadi-Farahani; A (December 2012). "Orthodontic considerations in restorative management of hypodontia patients with endosseous implants". Journal of Oral Implantology. 38 (6): 779–791. doi:10.1563/AAID-JOI-D-11-00022. PMID 21728818.
63. Al-Ani, Azza Husam; Antoun, Joseph Safwat; Thomson, William Murray; Merriman, Tony Raymond; Farella, Mauro (2017). "Hypodontia: An Update on Its Etiology, Classification, and Clinical Management". BioMed Research International. 2017: 1–9. doi:10.1155/2017/9378325. ISSN 2314-6133. PMC 5376450. PMID 28401166.
64. Ceyhan, Derya; Kirzioglu, Zuhal; Calapoglu, NiluferSahin (2014). "Mutations in the MSX1 gene in Turkish children with non-syndromic tooth agenesis and other dental anomalies". Indian Journal of Dentistry. 5 (4): 172–82. doi:10.4103/0975-962X.144717. ISSN 0975-962X. PMC 4260382. PMID 25565750.
65. Meaney, S.; Anweigi, L.; Ziada, H.; Allen, F. (2012-10-01). "The impact of hypodontia: a qualitative study on the experiences of patients". The European Journal of Orthodontics. 34 (5): 547–552. doi:10.1093/ejo/cjr061. ISSN 0141-5387. PMID 21693681.
66. J. A., Hobkirk; D., Gill; S. P., Jones (2011). Hypodontia A Team Approach to Management. Wiley. ISBN 978-1-405-18859-3.
67. Parkin, N.; Elcock, C.; Smith, R.N.; Griffin, R.C.; Brook, A.H. (2009-12-01). "The aetiology of hypodontia: The prevalence, severity and location of hypodontia within families". Archives of Oral Biology. 54: S52–S56. doi:10.1016/j.archoralbio.2008.11.002. ISSN 0003-9969. PMID 19100963.
68. SCHALK-VAN DER WEIDE, Y.; STEEN, W.H.A.; BOSMAN, F. (1993). "Taurodontism and length of teeth in patients with oligodontia". Journal of Oral Rehabilitation. 20 (4): 401–412. doi:10.1111/j.1365-2842.1993.tb01624.x. ISSN 0305-182X. PMID 8350175.
69. ^ Barber S, Bekker HL, Meads D, Pavitt S, Khambay B (February 2018). "Identification and appraisal of outcome measures used to evaluate hypodontia care: A systematic review" (PDF). American Journal of Orthodontics and Dentofacial Orthopedics. 153 (2): 184–194.e18. doi:10.1016/j.ajodo.2017.10.010. PMID 29407495. S2CID 20077787.
70. ^ Barber S, Bekker HL, Meads D, Pavitt S, Khambay B (February 2018). "Identification and appraisal of outcome measures used to evaluate hypodontia care: A systematic review" (PDF). American Journal of Orthodontics and Dentofacial Orthopedics. 153 (2): 184–194.e18. doi:10.1016/j.ajodo.2017.10.010. PMID 29407495. S2CID 20077787.
71. ^ Valle AL, Lorenzoni FC, Martins LM, Valle CV, Henriques JF, Almeida AL, Pegoraro LF (October 2011). "A multidisciplinary approach for the management of hypodontia: case report". Journal of Applied Oral Science. 19 (5): 544–8. doi:10.1590/S1678-77572011000500018. PMC 3984204. PMID 21986661.
72. ^ Hvaring CL, Øgaard B, Stenvik A, Birkeland K (February 2014). "The prognosis of retained primary molars without successors: infraocclusion, root resorption and restorations in 111 patients". European Journal of Orthodontics. 36 (1): 26–30. doi:10.1093/ejo/cjs105. hdl:10852/54811. PMID 23314329.
73. ^ Addy, Liam; Bishop, Karl; Knox, Jeremy (2006-12-02). "Modern Restorative Management of Patients with Congenitally Missing Teeth: 2. Orthodontic and Restorative Considerations". Dental Update. 33 (10): 592–595. doi:10.12968/denu.2006.33.10.592. ISSN 0305-5000. PMID 17209532.
74. Allen, P F; Witter, D J; Wilson, N H (November 1995). "The role of the shortened dental arch concept in the management of reduced dentitions". British Dental Journal. 179 (9): 355–357. doi:10.1038/sj.bdj.4808921. ISSN 0007-0610. PMID 7495632. S2CID 45670823.
75. ^ Jepson NJ, Nohl FS, Carter NE, Gillgrass TJ, Meechan JG, Hobson RS, Nunn JH (March 2003). "The interdisciplinary management of hypodontia: restorative dentistry". British Dental Journal. 194 (6): 299–304. doi:10.1038/sj.bdj.4809940. PMID 12682653.
76. Sletten DW, Smith BM, Southard KA, Casko JS, Southard TE (December 2003). "Retained deciduous mandibular molars in adults: a radiographic study of long-term changes". American Journal of Orthodontics and Dentofacial Orthopedics. 124 (6): 625–30. doi:10.1016/j.ajodo.2003.07.002. PMID 14666074.
77. Bjerklin K, Al-Najjar M, Kårestedt H, Andrén A (June 2008). "Agenesis of mandibular second premolars with retained primary molars: a longitudinal radiographic study of 99 subjects from 12 years of age to adulthood". European Journal of Orthodontics. 30 (3): 254–61. doi:10.1093/ejo/cjn027. PMID 18540014.
78. Ith-Hansen K, Kjaer I (June 2000). "Persistence of deciduous molars in subjects with agenesis of the second premolars". European Journal of Orthodontics. 22 (3): 239–43. doi:10.1093/ejo/22.3.239. PMID 10920556.
79. Powell, Laurie (2016-12-02). "Case study: management of a loose upper denture opposed by a shortened dental arch". Dental Update. 43 (10): 961–963. doi:10.12968/denu.2016.43.10.961. ISSN 0305-5000. PMID 29155537.
80. ^ Kiliaridis S, Sidira M, Kirmanidou Y, Michalakis K (2016). "Treatment options for congenitally missing lateral incisors". European Journal of Oral Implantology. 9 (Suppl 1): S5–24. PMID 27314109.
81. "Dental Update: Issue - Article: Hypodontia: Aesthetics and Functions Part 1: Aetiology and the Problems". www.dental-update.co.uk. Retrieved 2020-02-21.
82. ^ Rosa M, Zachrisson BU (April 2001). "Integrating esthetic dentistry and space closure in patients with missing maxillary lateral incisors". Journal of Clinical Orthodontics. 35 (4): 221–34. PMID 11345569.
83. ^ Kokich VO, Kinzer GA (2005). "Managing congenitally missing lateral incisors. Part I: Canine substitution". Journal of Esthetic and Restorative Dentistry. 17 (1): 5–10. doi:10.1111/j.1708-8240.2005.tb00076.x. PMID 15934680.
84. ^ Zachrisson BU, Rosa M, Toreskog S (April 2011). "Congenitally missing maxillary lateral incisors: canine substitution. Point". American Journal of Orthodontics and Dentofacial Orthopedics. 139 (4): 434–444. doi:10.1016/j.ajodo.2011.02.003. PMID 21457853.
85. Kinzer GA, Kokich VO (2005). "Managing congenitally missing lateral incisors. Part II: tooth-supported restorations". Journal of Esthetic and Restorative Dentistry. 17 (2): 76–84. doi:10.1111/j.1708-8240.2005.tb00089.x. PMID 16036123.
86. Kinzer GA, Kokich VO (2005). "Managing congenitally missing lateral incisors. Part III: single-tooth implants". Journal of Esthetic and Restorative Dentistry. 17 (4): 202–10. doi:10.1111/j.1708-8240.2005.tb00116.x. PMID 16231491.
87. ^ Filius MA, Cune MS, Raghoebar GM, Vissink A, Visser A (May 2016). "Prosthetic treatment outcome in patients with severe hypodontia: a systematic review". Journal of Oral Rehabilitation. 43 (5): 373–87. doi:10.1111/joor.12384. PMID 26899287.
88. Creugers NH, Käyser AF, Van't Hof MA (November 1992). "A seven-and-a-half-year survival study of resin-bonded bridges". Journal of Dental Research. 71 (11): 1822–5. doi:10.1177/00220345920710111101. PMID 1401445. S2CID 43374444.
89. Magnússon, T. E. (June 1984). "Hypodontia, hyperodontia, and double formation of primary teeth in Iceland. An epidemiological study". Acta Odontologica Scandinavica. 42 (3): 137–139. doi:10.3109/00016358408993864. ISSN 0001-6357. PMID 6332449.
90. ^ Stirrups, David (2005). "Hypodontia: A retrospective review of prevalence and etiology. Part I". Quintessence International. 36 (4): 263–70. PMID 15835422.
91. Nandhra, S. (2013-06-14). "Hypodontia: A Team Approach to Management (2010)". The European Journal of Orthodontics. 35 (5): 717. doi:10.1093/ejo/cjt039.
92. ^ Sisman, Yildiray; Uysal, Tancan; Gelgor, Ibrahim Erhan (July 2007). "Hypodontia. Does the Prevalence and Distribution Pattern Differ in Orthodontic Patients?". European Journal of Dentistry. 1 (3): 167–173. doi:10.1055/s-0039-1698333. ISSN 1305-7456. PMC 2638243. PMID 19212561.
93. ^ Sheikhi, Mahnaz; Sadeghi, Mohammad Ali; Ghorbanizadeh, Sajad (December 2012). "Prevalence of congenitally missing permanent teeth in Iran". Dental Research Journal. 9 (Suppl 1): 105–111. ISSN 1735-3327. PMC 3692187. PMID 23814548.
94. ^ Mukhopadhyay, Santanu; Mitra, Sanjib (2014). "Anomalies in primary dentition: Their distribution and correlation with permanent dentition". Journal of Natural Science, Biology, and Medicine. 5 (1): 139–143. doi:10.4103/0976-9668.127313. ISSN 0976-9668. PMC 3961919. PMID 24678213.
95. "Hypodontia—a Retrospective Review of Prevalence and Etiology. Part I". ResearchGate. Retrieved 2018-10-28.
96. Polder, Bart J.; Van't Hof, Martin A.; Van der Linden, Frans P. G. M.; Kuijpers-Jagtman, Anne M. (June 2004). "A meta-analysis of the prevalence of dental agenesis of permanent teeth". Community Dentistry and Oral Epidemiology. 32 (3): 217–226. doi:10.1111/j.1600-0528.2004.00158.x. ISSN 0301-5661. PMID 15151692.

External links

• Developmental tooth disorders