Hubbry Logo
Hard palateHard palateMain
Open search
Hard palate
Community hub
Hard palate
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Contribute something
Hard palate
Hard palate
Hard palate
View on Wikipedia
from Wikipedia
Hard palate
Mouth (oral cavity)
Upper respiratory system, with hard palate labeled at right
Details
ArteryGreater palatine artery
NerveGreater palatine nerve, nasopalatine nerve
Identifiers
Latinpalatum durum
MeSHD021362
TA98A05.1.01.103
TA22779
FMA55023
Anatomical terminology

The hard palate is a thin horizontal bony plate made up of two bones of the facial skeleton, located in the roof of the mouth. The bones are the palatine process of the maxilla and the horizontal plate of palatine bone. The hard palate spans the alveolar arch formed by the alveolar process that holds the upper teeth (when these are developed).

Structure

[edit]

The hard palate is formed by the palatine process of the maxilla and horizontal plate of palatine bone. It forms a partition between the nasal passages and the mouth. On the anterior portion of the hard palate are the plicae, irregular ridges in the mucous membrane that help hold food while the teeth are biting into it while also facilitating the movement of food backward towards the larynx once pieces have been bitten off. This partition is continued deeper into the mouth by a fleshy extension called the soft palate.

On the ventral surface of the hard palate, some projections or transverse ridges are present which are called palatine rugae.[1]

Function

[edit]

The hard palate is important for feeding and speech. Mammals with a defective hard palate may die shortly after birth due to inability to suckle. It is also involved in mastication in many species. The interaction between the tongue and the hard palate is essential in the formation of certain speech sounds, notably high-front vowels, palatal consonants, and retroflex consonants such as [i] like "see", [j] like "yes", [ç] (realization of /hj/ in English) like "hue", and [ɻ] (/r/, only for some speakers) like "red".

Clinical significance

[edit]

Cleft palate

[edit]

In the birth defect called cleft palate, the left and right portions of this plate are not joined, forming a gap between the mouth and nasal passage (a related defect affecting the face is cleft lip).

While a cleft palate has a severe impact upon the ability to nurse and speak, it is now successfully treated through reconstructive surgical procedures at an early age. This is the time where such procedures are available.

Due to the complexity of this birth defect, researchers still do not know exactly what causes the cleft palate to form during foetal development. Recently, these researchers found that even though there is no exact cause, there are several factors that drastically increase the risk of a baby being born with an orofacial cleft palate. As for the environmental risk factors, maternal smoking is the most influential risk factor. Based on a recent study of 103 German patients with cleft palates, it was found that 25.2% of their mothers smoked during pregnancy, a higher proportion than for the population as a whole.[2]

While maternal smoking during pregnancy is a risk, there are also several genetic risk factors. Six single-nucleotide polymorphisms in the PAX7 gene are implicated in the development of facial features.[3] These variations occur at six loci: 1p36, 2p21, 3p11.1, 8q21.3, 13q31.1 and 15q22.[3] When tested in the European and Asian communities, five of the six loci had a significant association at the 95% confidence level.[3] Besides the PAX 7 gene variants, there were also five possible mutations found in the transforming growth factor-alpha gene (TGFA) that could lead to the development of a cleft palate.[4] Even though several risk factors have been linked to cleft palates, more research must be done in order to determine the true causes of the defect.

Palatal abscess

[edit]

Palatal abscesses may also occur.[5]

Hard palate pigmentation

[edit]

Long-term use of the drug chloroquine diphosphatase, used in malaria prophylaxis, rheumatoid arthritis and other conditions, was found to cause bluish-grey pigmentation in the hard palate.[6][7]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Hard palate

View on Grokipedia
from Grokipedia
The hard palate is the anterior, bony portion of the roof of the , comprising approximately two-thirds of the total and serving as a rigid partition between the oral and nasal cavities. Structurally, it consists of the palatine processes of the bones anteriorly and the horizontal plates of the palatine bones posteriorly, which fuse along the midline to form a stable bony framework covered by mucoperiosteum. The inferior (oral) surface features and transverse ridges known as rugae palatinae, which assist in manipulation, while the superior (nasal) surface is lined with ciliated to support respiratory functions. Functionally, the hard palate provides essential structural support for the , facilitates mastication and deglutition by aiding bolus formation and propulsion, and contributes to by forming a resonant chamber for speech sounds. Its development occurs embryologically as part of the secondary palate between the 6th and 12th weeks of , with fusion to the primary palate completing by the 9th week to establish the definitive oral-nasal separation. The hard palate receives its primary blood supply from the greater palatine arteries, branches of the , with additional contributions from the ascending palatine artery; venous drainage parallels this via corresponding veins. Sensory innervation is provided by the greater and lesser palatine nerves, along with the nasopalatine nerve, all deriving from the maxillary division of the (CN V2), ensuring tactile and pain sensation across the region. Clinically, the hard palate is notable for its involvement in congenital anomalies such as cleft palate, the third most common , and as a site for malignancies including .

Anatomy

Bony Structure

The hard palate forms the anterior bony portion of the roof of the oral cavity, composed primarily of the palatine processes of the anteriorly and the horizontal plates of the bones posteriorly. These structures fuse along the midline palatine suture, creating a rigid framework that separates the oral and nasal cavities and spans the anterior two-thirds of the total palatal length. In adults, the hard palate typically measures about 40–50 mm in anteroposterior length—from the posterior aspect of the teeth to the posterior border—and 35–45 mm in transverse width at its broadest point, with a slight vaulted or arched shape that enhances its mechanical stability. The anterior and lateral borders are contiguous with the maxillary alveolar processes and the dental arches, providing support for the upper teeth, while the posterior border, formed by the free edge of the horizontal plates of the palatine bones, transitions smoothly to the at the level of the posterior nasal spine in the midline. Key openings in the bony structure include the incisive foramen, located in the anterior midline just posterior to the central incisors, which transmits the nasopalatine nerve and branches of the sphenopalatine vessels. More posteriorly, the lies near the last maxillary molar, serving as the exit for the greater palatine neurovascular bundle, while the lesser palatine foramina, situated immediately behind it on the pyramidal process of the , accommodate the lesser palatine nerves and vessels. These foramina are critical landmarks for the passage of structures supplying the palatal region.

Mucosa and Surface Features

The mucosa of the hard palate consists of distinct epithelial layers on its inferior (oral) and superior (nasal) surfaces, along with characteristic surface features that contribute to its functional . The inferior surface is covered by a stratified squamous keratinized , characteristic of masticatory mucosa, which provides durability against mechanical stresses from mastication. This overlays a rich in , supporting the palatal and other landmarks. Prominent transverse ridges known as palatine traverse the anterior two-thirds of the oral surface, most pronounced in the front near the alveolar processes, where they number three to five on each side. These facilitate food manipulation and bolus formation during by increasing surface . Running along the midline of the oral surface is the palatine raphe, a subtle longitudinal ridge extending from the anteriorly to the junction with the posteriorly, marking the line of embryonic fusion of the palatal shelves. Anterior to the incisive foramen, the appears as a small, pear-shaped elevation of mucosa, serving a sensory function through dense innervation that contributes to oral tactile . Embedded within the of the oral surface are numerous minor salivary glands, predominantly of the mucous type, which are more concentrated in the posterior region to provide and . In contrast, the superior (nasal) surface of the hard palate is lined with ciliated , continuous with the mucosa, facilitating in the . Physiological pigmentation of the hard palatal mucosa varies by racial background, often appearing darker in individuals of African or Asian descent due to increased melanin production in melanocytes, representing a normal variant rather than .

Neurovascular Supply

The hard palate receives sensory innervation solely from branches of the maxillary division (V2) of the (cranial nerve V), as it lacks and therefore has no motor innervation. The emerges from the to supply sensation to the mucosa and gingiva of the anterior two-thirds of the hard palate, coursing anteriorly beneath the mucosal surface. The lesser palatine nerves exit through the lesser palatine foramina to innervate the posterior aspect of the hard palate mucosa. In the anterior midline, the nasopalatine nerve, traveling through the incisive canal, provides sensory input to the palatal mucosa adjacent to the central incisors. Arterial supply to the hard palate is predominantly from the , a terminal branch of the (itself derived from the ), which enters the palate via the and proceeds anteriorly to anastomose with other vessels. This artery nourishes the bulk of the palatal mucosa, glands, and underlying bone. Supplemental perfusion is provided by the , a maxillary artery branch that contributes to the anterior hard palate through the incisive canal alongside the nasopalatine nerve, and by the ascending palatine artery, originating from the , which supplies the posterolateral regions via ascending branches. Venous drainage from the hard palate follows the arterial pathways in reverse, with the greater and lesser palatine veins collecting blood and emptying into the pterygoid venous plexus, which ultimately connects to the . Lymphatic vessels from the hard palate drain primarily to the retropharyngeal nodes and the deep cervical chain, facilitating immune surveillance of the oral and interface.

Embryology and Development

Formation of the Palate

The formation of the hard palate occurs during early embryonic development through a series of coordinated morphogenetic events involving the primary and secondary palates. The primary palate begins to form around the 6th week of from the fusion of the medial nasal prominences, which are part of the frontonasal prominence, with the maxillary prominences. This fusion creates the intermaxillary segment, comprising the (anterior hard palate), the , and the primitive nasal floor, effectively separating the oral and nasal cavities anteriorly. The secondary , which constitutes the of the hard , develops concurrently from the 6th to 12th weeks, originating from paired palatine shelves that protrude from the maxillary prominences. Initially positioned vertically alongside the , these shelves undergo rapid elevation to a horizontal orientation by the 8th-9th week, facilitated by tongue depression and remodeling. Fusion commences anteriorly around the 9th week, where the shelves meet in the midline and adhere to the primary ; this progresses posteriorly, with the posterior shelves also fusing superiorly to the by the 12th week. The epithelial seams at contact points undergo programmed breakdown—via , migration, and epithelial-mesenchymal transformation—allowing mesenchymal tissues to unite and form a continuous midline structure. These processes are tightly regulated by molecular signaling pathways that ensure proper shelf growth, , and fusion. Transforming growth factor-β (TGF-β) signaling, particularly TGF-β3, is crucial for medial edge epithelial adhesion and seam degeneration, activating Smad2/3 and p38 MAPK pathways to promote exit and in the epithelial layer. Sonic hedgehog (Shh) signaling drives palatal shelf outgrowth and by regulating mesenchymal proliferation through interactions with factors like and Foxf transcription factors, while also coordinating epithelial-mesenchymal signaling for patterning. Palate formation integrates with broader facial development during weeks 4-7, as the frontonasal and maxillary processes—derived largely from cells—undergo growth and fusion to establish the midface architecture, with the palatine shelves emerging as lateral extensions of the maxillary prominences.

Ossification

The ossification of the hard palate proceeds via , a process in which mesenchymal condensations derived from cells directly differentiate into osteoblasts without an intervening stage, beginning around the 8th week of with multiple centers in the palatine processes of the and the horizontal plates of the bones. In the maxillary component, ossification initiates from a single center positioned near the incisive foramen, with bone formation progressively extending posteriorly to form the anterior two-thirds of the hard palate. The posterior portion, contributed by the horizontal plates of the palatine bones, develops through a single ossification center located at the junction of the horizontal and perpendicular plates, with ossification spreading medially, downward into the pyramidal process, and upward into the vertical part, resulting in completion of primary ossification by birth. Postnatally, the hard palate undergoes minor remodeling driven by surface and resorption to accommodate facial growth, achieving full structural maturity by late childhood, with the entire process lacking any component.

Function

Mechanical Support

The hard palate serves as a rigid partition, forming the floor of the and the roof of the oral cavity, thereby maintaining separation between these two spaces to facilitate independent respiratory and digestive functions. The hard palate maintains this partition, while the elevates during to prevent the reflux of food or liquids into the nasopharynx, ensuring that the bolus is directed solely toward the without nasal contamination. By providing this impermeable divide, the hard palate enables simultaneous through the and oral processing of food, a critical for efficient alimentation. In mastication, the hard palate distributes occlusal forces transmitted from the teeth, offering a stable bony platform against which the compresses and manipulates particles. The transverse , irregular ridges on its anterior surface, enhance this process by providing to aid in bolus formation and posterior propulsion of the mass toward the oropharynx. These , covered by mechanical papillae, help retain and shape the bolus, optimizing its consistency for safe swallowing while minimizing spillage. During suckling in infants, the hard palate plays a pivotal role in generating an airtight seal with the , creating a essential for extracting from the . The 's compression against the hard palate strips and expresses the liquid, a mechanism vital for nutritive feeding in early life; defects such as cleft palate can impair this function, leading to feeding difficulties. As part of the , the hard palate integrates seamlessly with the via its palatine processes and with the through articulations of the bones, contributing to overall cranial stability and midfacial structural integrity. This bony framework supports the upper and resists deformative forces from mastication, anchoring the viscerocranium to the for balanced biomechanical load distribution.

Role in Speech and Swallowing

The hard palate serves as a stable, immovable surface essential for articulation during , particularly for consonants involving alveolar and velar contacts such as /t/, /d/, and /k/ , where the tip or dorsum presses against it to create necessary occlusions and releases. This rigid structure provides a consistent articulatory boundary, enabling precise modulation of and in the oral cavity. Defects in the hard palate can lead to by allowing unintended nasal , underscoring its role in maintaining oral-nasal separation during . In swallowing, the hard palate facilitates bolus propulsion as the tongue elevates and compresses against it, directing the food or liquid posteriorly toward the oropharynx in a coordinated peristaltic motion. This contact seals the bolus posteriorly during the oral preparatory phase and supports efficient transit by providing a firm posterior boundary, with the elevating simultaneously to close the nasopharynx and prevent nasal regurgitation. The pattern of tongue pressure on the hard palate during deglutition ensures smooth bolus flow, with the highest peak pressures typically occurring at the anteriomedian part of the hard palate. Sensory feedback from the palatine nerves, including the greater and lesser palatine branches of the , detects pressure and touch on the hard palate, providing proprioceptive input critical for modulating movements in both speech articulation and coordination. This somatosensory information relays to central neural centers, enabling real-time adjustments to ensure accurate production and safe bolus transit without aspiration. Loss of this palatal sensation, as seen in localized studies, disrupts swallowing kinematics and oral motor control. Evolutionarily, the hard palate has adapted alongside vocal tract modifications to support complex , with its domed shape and the tongue's increased flexibility allowing deformation against it for producing quantal vowels like /i/ and /u/ as well as velar consonants, capabilities limited in other mammals whose flatter palates and less versatile tongues prioritize feeding over articulate speech. This adaptation likely emerged in around 250,000–350,000 years ago, enhancing communicative efficiency beyond the ingestive functions dominant in nonhuman .

Clinical Significance

Congenital Anomalies

Congenital anomalies of the hard palate primarily involve developmental malformations arising from incomplete fusion during embryonic development. The most common is cleft palate, which results from the failure of the primary and secondary palatal shelves to fuse properly between the 6th and 12th weeks of . This condition occurs in approximately 1 in 1,500 live births worldwide, with isolated cleft palate (without cleft lip) being less frequent than combined cleft lip and palate forms. Clefts affecting the hard palate can occur in isolation or in combination with cleft lip, presenting as unilateral or bilateral variants that extend from the incisive foramen posteriorly. The etiology of cleft palate is multifactorial, involving genetic, environmental, and syndromic factors. Genetic contributions include mutations in the IRF6 gene, which account for up to 12% of the genetic risk for nonsyndromic cleft lip with or without palate and increase recurrence risk threefold in affected families. Environmental influences, such as maternal during , elevate the risk by 1.3- to 2-fold through mechanisms like vascular disruption and reduced placental blood flow. in early also heightens susceptibility, with periconceptional supplementation reducing nonsyndromic oral cleft risk by up to 50%. Syndromic associations are common in approximately 50% of cleft palate cases, notably (featuring micrognathia, glossoptosis, and cleft palate), often requiring multidisciplinary management. Consequences of hard palate clefts include significant functional impairments. Feeding difficulties arise from the inability to create an oral-nasal seal, leading to nasal regurgitation, poor , and aspiration risk in infancy. Recurrent and result from due to abnormal insertion. Speech development is compromised by velopharyngeal insufficiency, causing hypernasal and articulation errors, though detailed mechanisms are addressed in discussions of palatal roles in . Surgical intervention via palatoplasty, typically performed between 6 and 12 months of age, reconstructs the palate using techniques like von Langenbeck or two-flap methods to restore separation of oral and nasal cavities and optimize long-term outcomes. Milder variants include bifid uvula and submucous cleft palate, which represent incomplete of fusion defects. A bifid uvula, a split in the uvular midline, occurs in up to 2-5% of the population and serves as a potential marker for underlying submucous cleft palate, as it is present in approximately 30% of such cases. Submucous clefts involve a bony notch at the hard palate's posterior border and diastasis of levator veli palatini muscles beneath intact mucosa, potentially leading to occult velopharyngeal dysfunction if untreated. These anomalies often require vigilant monitoring for speech and feeding issues, with surgical correction considered if functional deficits emerge.

Inflammatory and Infectious Conditions

Inflammatory and infectious conditions of the hard palate encompass a range of acquired pathologies that can cause discomfort, ulceration, or structural changes, often requiring prompt diagnosis to distinguish them from more serious diseases. These conditions typically arise from local trauma, microbial invasion, or systemic factors, affecting the mucosal or bony components of the palate. Palatal abscesses are a common infectious complication originating from odontogenic sources, where infection from maxillary teeth spreads through the bone to form a pus-filled collection in the palatal mucosa. This spread occurs via the vascular and lymphatic pathways of the maxilla, leading to localized swelling, severe pain, and potential fluctuance over the hard palate. Treatment involves incision and drainage of the abscess, along with addressing the underlying dental pathology through root canal therapy or extraction, and systemic antibiotics to resolve the infection. Fungal infections, particularly candidiasis (oral thrush), frequently involve the hard palate in immunocompromised individuals, presenting as adherent white plaques that can be scraped off, revealing an erythematous base. Caused by overgrowth of Candida albicans, these lesions result from disrupted mucosal barriers or reduced host immunity, with the hard and soft palates among the common sites affected. Syphilitic infections of the hard palate occur in primary, secondary, or tertiary stages of the disease; primary chancres appear as painless ulcers, while secondary syphilis may cause mucous patches or shallow erosions, and tertiary gummas form granulomatous, destructive lesions that can perforate the palate. These manifestations stem from Treponema pallidum invasion, often mimicking other ulcerative conditions. Human papillomavirus (HPV) infections lead to benign papillary lesions such as squamous papillomas or warts on the hard palate, characterized by exophytic, verrucous growths induced by viral proliferation in the stratified epithelium. These are typically asymptomatic but may require excision if symptomatic or for diagnostic confirmation. Non-infectious inflammatory conditions include , a benign bony arising in the midline of the hard palate, often bilateral and asymptomatic unless it grows large enough to interfere with denture fit or cause ulceration from trauma. This developmental variant is prevalent in up to 27% of adults and requires no treatment unless symptomatic, in which case surgical removal may be considered. is a rare, self-limiting inflammatory disorder of the minor salivary glands in the hard palate, presenting as a firm swelling that ulcerates and mimics due to and of ductal . It typically resolves spontaneously within 4-10 weeks without intervention, though observation is essential to rule out . Diagnosis of these conditions relies on clinical examination, with recommended for persistent or atypical lesions to confirm and exclude neoplasia; for instance, incisional reveals pseudoepitheliomatous hyperplasia in or fungal hyphae in . Risk factors include poor , which predisposes to odontogenic abscesses and bacterial overgrowth, and (e.g., from , , or ), which heightens susceptibility to opportunistic infections like or syphilis reactivation. Early intervention prevents complications such as palatal perforation or secondary bacteremia.

Neoplastic Conditions

Neoplastic conditions of the hard palate encompass both benign and malignant tumors arising from its mucosal, glandular, or connective tissues. Benign neoplasms are typically slow-growing and localized, while malignant ones often exhibit aggressive behavior with potential for local invasion and . These conditions require histopathological confirmation for , as clinical features can overlap with other palatal pathologies. Benign tumors of the hard palate most commonly include , a slow-growing originating from minor salivary glands, characterized by a firm, submucosal mass without ulceration. This tumor accounts for the majority of benign palatal lesions and is managed with to prevent recurrence due to its potential for local aggressiveness despite lacking a complete capsule. Squamous papilloma, another benign entity, presents as a painless, exophytic, cauliflower-like growth linked to human papillomavirus (HPV) infection, particularly types 6 and 11, and is treated via conservative excision. Malignant tumors predominate in the hard palate's neoplastic pathology, with squamous cell carcinoma (SCC) being the most common, representing the primary epithelial malignancy and often associated with and alcohol use as key risk factors. Salivary gland-derived malignancies, such as and , also occur frequently in this region due to the abundance of minor salivary glands, exhibiting and variable grading that influences . Clinical typically involves an ulcerated or exophytic mass, pain, oral bleeding, halitosis, or ill-fitting , with advanced cases showing bony erosion or nasal obstruction. Staging follows the TNM classification for oral cavity cancers, guiding multidisciplinary management. Treatment for malignant hard palate tumors emphasizes surgical resection with wide margins, potentially involving partial or total maxillectomy for local control, often combined with postoperative ; chemotherapy is reserved for advanced or metastatic disease. Five-year survival rates for early-stage SCC range from 50% to 70%, varying by tumor grade, margins, and nodal involvement, though tumors like have lower long-term survival due to late recurrences. Rare pigmented lesions include mucosal , presenting as irregular, darkly pigmented macules with rapid growth and poor (5-year survival <20%), treated with wide excision and , and Kaposi , an HIV-associated appearing as reddish-purple plaques responsive to antiretroviral therapy and localized .

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK557817/
  2. https://pmc.ncbi.nlm.nih.gov/articles/PMC6369495/
  3. https://www.ncbi.nlm.nih.gov/books/NBK572115/
  4. https://www.kenhub.com/en/library/anatomy/hard-palate
  5. https://www.ncbi.nlm.nih.gov/books/NBK538325/
  6. https://head-face-med.biomedcentral.com/articles/10.1186/1746-160X-10-8
  7. https://medicine.uams.edu/neuroscience/education/medical-school-courses/human-structure-module/anatomy-tables/nerve-tables/nerves-of-the-head-and-neck/
  8. https://medicine.uams.edu/neuroscience/education/medical-school-courses/human-structure-module/anatomy-tables/artery-tables/arteries-of-the-head-and-neck/
  9. https://www.ncbi.nlm.nih.gov/books/NBK513317/
  10. https://www.ncbi.nlm.nih.gov/books/NBK545202/
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC10234451/
  12. https://journals.biologists.com/dev/article/139/2/231/45401/Palatogenesis-morphogenetic-and-molecular
  13. https://pmc.ncbi.nlm.nih.gov/articles/PMC5613875/
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC3243091/
  15. https://www.bartleby.com/lit-hub/anatomy-of-the-human-body/5b-5-the-palatine-bone/
  16. https://www.kenhub.com/en/library/anatomy/the-maxilla
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC7966493/
  18. https://pubmed.ncbi.nlm.nih.gov/18266285/
  19. https://www.ajnr.org/content/35/1/10
  20. https://www.ncbi.nlm.nih.gov/books/NBK545271/
  21. https://pubmed.ncbi.nlm.nih.gov/16434740/
  22. https://www.sciencedirect.com/topics/medicine-and-dentistry/hard-palate
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC4530609/
  24. https://www.kenhub.com/en/library/anatomy/the-viscerocranium
  25. https://pmc.ncbi.nlm.nih.gov/articles/PMC3885355/
  26. https://pmc.ncbi.nlm.nih.gov/articles/PMC7866712/
  27. https://www.ncbi.nlm.nih.gov/books/NBK541071/
  28. https://www.ncbi.nlm.nih.gov/books/NBK554405/
  29. https://pubmed.ncbi.nlm.nih.gov/15667061/
  30. https://pmc.ncbi.nlm.nih.gov/articles/PMC10052750/
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC4319539/
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC10266234/
  33. https://publications.aap.org/pediatricsinreview/article/45/11/625/199699/Cleft-Lip-and-Palate-and-Isolated-Cleft-Palate
  34. https://www.ncbi.nlm.nih.gov/books/NBK563128/
  35. https://www.nejm.org/doi/full/10.1056/NEJMoa032909
  36. https://publications.aap.org/aapgrandrounds/article/3/6/61/85944/Prenatal-Smoking-Increases-Risk-of-Cleft-Lip
  37. https://www.nature.com/articles/s41598-021-91825-9
  38. https://pediatric-ent.com/cleft-palate-repair-palatoplasty/
  39. https://www.healthline.com/health/bifid-uvula
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC2634784/
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC12428685/
  42. https://www.ncbi.nlm.nih.gov/books/NBK545282/
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC4681845/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC5911365/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC9231211/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC2811633/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC10246509/
  48. https://pmc.ncbi.nlm.nih.gov/articles/PMC4260387/
  49. https://my.clevelandclinic.org/health/diseases/24829-torus-palatinus
  50. https://pmc.ncbi.nlm.nih.gov/articles/PMC4059586/
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC9884392/
  52. https://pubmed.ncbi.nlm.nih.gov/17044429/
  53. https://www.ncbi.nlm.nih.gov/books/NBK594246/
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC11383258/
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC3645400/
  56. https://www.ncbi.nlm.nih.gov/books/NBK564515/
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC10135659/
  58. https://pmc.ncbi.nlm.nih.gov/articles/PMC7773679/
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC7948021/
  60. https://pmc.ncbi.nlm.nih.gov/articles/PMC5839449/
  61. https://pubmed.ncbi.nlm.nih.gov/23679875/
Add your contribution
Related Hubs
Contribute something
User Avatar
No comments yet.