As many as 50–70% of people who survive traffic accidents have facial trauma. In most developed countries, violence from other people has replaced vehicle collisions as the main cause of maxillofacial trauma; however in many developing countries traffic accidents remain the major cause. Increased use of seat belts and airbags has been credited with a reduction in the incidence of maxillofacial trauma, but fractures of the mandible (the jawbone) are not decreased by these protective measures. The risk of maxillofacial trauma is decreased by a factor of two with use of motorcycle helmets. A decline in facial bone fractures due to vehicle accidents is thought to be due to seat belt and drunk driving laws, strictly enforced speed limits and use of airbags. In vehicle accidents, drivers and front seat passengers are at highest risk for facial trauma.

Facial fractures are distributed in a fairly normal curve by age, with a peak incidence occurring between ages 20 and 40, and children under 12 suffering only 5–10% of all facial fractures. Most facial trauma in children involves lacerations and soft tissue injuries. There are several reasons for the lower incidence of facial fractures in children: the face is smaller in relation to the rest of the head, children are less often in some situations associated with facial fractures such as occupational and motor vehicle hazards, there is a lower proportion of cortical bone to cancellous bone in children's faces, poorly developed sinuses make the bones stronger, and fat pads provide protection for the facial bones.

Head and brain injuries are commonly associated with facial trauma, particularly that of the upper face; brain injury occurs in 15–48% of people with maxillofacial trauma. Coexisting injuries can affect treatment of facial trauma; for example they may be emergent and need to be treated before facial injuries. People with trauma above the level of the collar bones are considered to be at high risk for cervical spine injuries (spinal injuries in the neck) and special precautions must be taken to avoid movement of the spine, which could worsen a spinal injury.

Injury mechanisms such as falls, assaults, sports injuries, and vehicle crashes are common causes of facial trauma in children as well as adults. Blunt assaults, blows from fists or objects, are a common cause of facial injury. Facial trauma can also result from wartime injuries such as gunshots and blasts.

Animal attacks and work-related injuries such as industrial accidents are other causes. Vehicular trauma is one of the leading causes of facial injuries. Trauma commonly occurs when the face strikes a part of the vehicle's interior, such as the steering wheel. In addition, airbags can cause corneal abrasions and lacerations (cuts) to the face when they deploy.

Bone stability after a fracture occurs between 3 and 4 weeks. Some experts suggest not wearing glasses or blowing the nose during this time as it can affect the bone alignment. Full bone fusion occurs between 4 and 8 weeks. General activity is fine after 1–2 weeks, but contact sports are not advisable for at least 2–3 months, depending on the extent of injury. It is recommended that when participating in sports a face guard should be worn for at least 6 weeks post-injury.

Acute injury to the internal carotid artery (carotid dissection, occlusion, pseudoaneurysm formation) may be asymptomatic or result in life-threatening bleeding. They are almost exclusively observed when the carotid canal is fractured, although only a minority of carotid canal fractures result in vascular injury. Involvement of the petrous segment of the carotid canal is associated with a relatively high incidence of carotid injury.

A compound elevated skull fracture is a rare type of skull fracture where the fractured bone is elevated above the intact outer table of the skull. This type of skull fracture is always compound in nature. It can be caused during an assault with a weapon where the initial blow penetrates the skull and the underlying meninges and, on withdrawal, the weapon lifts the fractured portion of the skull outward. It can also be caused the skull rotating while being struck in a case of blunt force trauma, the skull rotating while striking an inanimate object as in a fall, or it may occur during transfer of a patient after an initial compound head injury.

The healing time for a routine mandible fractures is 4–6 weeks whether MMF or rigid internal fixation (RIF) is used. For comparable fractures, patients who received MMF will lose more weight and take longer to regain mouth opening, whereas, those who receive RIF have higher infection rates.

The most common long-term complications are loss of sensation in the mandibular nerve, malocclusion and loss of teeth in the line of fracture. The more complicated the fracture (infection, comminution, displacement) the higher the risk of fracture.

Condylar fractures have higher rates of malocclusion which in turn are dependent on the degree of displacement and/or dislocation. When the fracture is intracapsular there is a higher rate of late-term osteoarthritis and the potential for ankylosis although the later is a rare complication as long as mobilization is early. Pediatric condylar fractures have higher rates of ankylosis and the potential for growth disturbance.

Rarely, mandibular fracture can lead to Frey's syndrome.

Mandible fracture causes vary by the time period and the region studied. In North America, blunt force trauma (a punch) is the leading cause of mandible fracture whereas in India, motor vehicle collisions are now a leading cause. On battle grounds, it is more likely to be high velocity injuries (bullets and shrapnel). Prior to the routine use of seat belts, airbags and modern safety measures, motor vehicle collisions were a leading cause of facial trauma. The relationship to blunt force trauma explains why 80% of all mandible fractures occur in males. Mandibular fracture is a rare complication of third molar removal, and may occur during the procedure or afterwards. With respect to trauma patients, roughly 10% have some sort of facial fracture, the majority of which come from motor vehicle collisions. When the person is unrestrained in a car, the risk of fracture rises 50% and when an unhelmeted motorcyclist the risk rises 4-fold.

Nasal fractures are caused by physical trauma to the face. Common sources of nasal fractures include sports injuries, fighting, falls, and car accidents in the younger age groups, and falls from syncope or impaired balance in the elderly.

A fracture in conjunction with an overlying laceration that tears the epidermis and the meninges—or runs through the paranasal sinuses and the middle ear structures, putting the outside environment in contact with the cranial cavity—is a compound fracture.

Compound fractures may either be clean or contaminated. Intracranial air (pneumocephalus) may occur in compound skull fractures.

The most serious complication of compound skull fractures is infection. Increased risk factors for infection include visible contamination, meningeal tear, loose bone fragments and presenting for treatment more than eight hours after initial injury.

Non-displaced fractures usually heal without intervention. Patients with basilar skull fractures are especially likely to get meningitis. Unfortunately, the efficacy of prophylactic antibiotics in these cases is uncertain.

A zygoma fracture (zygomatic fracture) is a form of facial fracture caused by a fracture of the zygomatic bone. A zygoma fracture is often the result of facial trauma such as violence, falls or automobile accidents.

Symptoms include flattening of the face, trismus (reduced opening of the jaw) and lateral subconjunctival hemorrhage.

A Le Fort fracture of the skull is a classic transfacial fracture of the midface, involving the maxillary bone and surrounding structures in either a horizontal, pyramidal or transverse direction. The hallmark of Lefort fractures is traumatic "pterygomaxillary separation", which signifies fractures between the pterygoid plates, horseshoe shaped bony protuberances which extend from the inferior margin of the maxilla, and the maxillary sinuses. Continuity of this structure is a keystone for stability of the midface, involvement of which impacts surgical management of trauma victims, as it requires fixation to a horizontal bar of the frontal bone. The pterygoid plates lie posterior to the upper dental row, or alveolar ridge, when viewing the face from an anterior view. The fractures are named after French surgeon René Le Fort (1869–1951), who discovered the fracture patterns by examining crush injuries in cadavers.

Common causes of head injury are motor vehicle traffic collisions, home and occupational accidents, falls, and assaults. Wilson's disease has also been indicative of head injury. According to the United States CDC, 32% of traumatic brain injuries (another, more specific, term for head injuries) are caused by falls, 10% by assaults, 16.5% by being struck or against something, 17% by motor vehicle accidents, 21% by other/unknown ways. In addition, the highest rate of injury is among children ages 0–14 and adults age 65 and older.

Lefort I - Slight swelling of the upper lip, ecchymosis is present in the buccal sulcus beneath each zygomatic arch, malocclusion, mobility of teeth. Impacted type of fractures may be almost immobile and it is only by grasping the maxillary teeth and applying a little firm pressure that a characteristic grate can be felt which is diagnostic of the fracture. Percussion of upper teeth results in cracked pot sound. Guérin's sign is present characterised by ecchymosis in the region of greater palatine vessels.

Lefort II and Lefort III (common) - Gross edema of soft tissue over the middle third of the face, bilateral circumorbital ecchymosis, bilateral subconjunctival hemorrhage, epistaxis, CSF rhinorrhoea, dish face deformity, diplopia, enophthalmos, cracked pot sound.

Lefort II - Step deformity at infraorbital margin, mobile mid face, anesthesia or paresthesia of cheek.

Lefort III - Tenderness and separation at frontozygomatic suture, lengthening of face, depression of ocular levels (enophthalmos), hooding of eyes, and tilting of occlusal plane, an imaginary curved plane between the edges of the incisors and the tips of the posterior teeth. As a result, there is gagging on the side of injury.

In children with uncomplicated minor head injuries the risk of intra cranial bleeding over the next year is rare at 2 cases per 1 million. In some cases transient neurological disturbances may occur, lasting minutes to hours. Malignant post traumatic cerebral swelling can develop unexpectedly in stable patients after an injury, as can post traumatic seizures. Recovery in children with neurologic deficits will vary. Children with neurologic deficits who improve daily are more likely to recover, while those who are vegetative for months are less likely to improve. Most patients without deficits have full recovery. However, persons who sustain head trauma resulting in unconsciousness for an hour or more have twice the risk of developing Alzheimer's disease later in life.

Head injury may be associated with a neck injury. Bruises on the back or neck, neck pain, or pain radiating to the arms are signs of cervical spine injury and merit spinal immobilization via application of a cervical collar and possibly a long board.If the neurological exam is normal this is reassuring. Reassessment is needed if there is a worsening headache, seizure, one sided weakness, or has persistent vomiting.

To combat overuse of Head CT Scans yielding negative intracranial hemorrhage, which unnecessarily expose patients to radiation and increase time in the hospital and cost of the visit, multiple clinical decision support rules have been developed to help clinicians weigh the option to scan a patient with a head injury. Among these are the Canadian Head CT rule, the PECARN Head Injury/Trauma Algorithm, and the New Orleans/Charity Head Injury/Trauma Rule all help clinicians make these decisions using easily obtained information and noninvasive practices.

Ocular trauma is the fourth most common injury sustained in military combat today. In a pool of 387 randomly selected soldiers injured by blast trauma in Operation Iraqi Freedom, 329 (89%) sustained ocular trauma. Emergency treatment of resulting injuries falls under the realm of emergency care and effective patient triage, often incorporating protocols for blunt and penetrating trauma. As a result, physicians have devised a concise algorithm for the treatment of patients with ocular injuries secondary to blast trauma.

Visual outcomes for patients with ocular trauma due to blast injuries vary, and prognoses depend upon the type of injury sustained. The majority of poor visual outcomes arise from perforating injuries: only 21% of patients with perforating injuries with pre-operative light perception had a final best-corrected visual acuity (BCVA) better than 20/200. Collectively, patients who experienced choroidal hemorrhage, perforated or penetrated globes, retinal detachment, traumatic optic neuropathy, and subretinal macular hemorrhage carried the highest incidence rates of BCVAs worse than 20/200. Reports from Operation Iraqi Freedom (OIF) indicate that 42% of soldiers with globe injuries of any kind had a BCVA greater than or equal to 20/40 six months after injury, and soldiers with intraocular foreign bodies (IOFBs) retained 20/40 or better vision in 52% of studied cases.

Globe perforation, oculoplastic intervention, and neuro-ophthalmic injuries contribute significantly to reported poor visual outcomes. 21% of tertiary centers treating patients exposed to blast trauma reported traumatic optic neuropathy (TON) in their patients, although avulsion of the optic nerve and TON were reported in only 3% of combat injuries. In the event that a victim of globe penetrating trauma cannot perceive any light within two weeks of surgical intervention, the ophthalmologist may choose to enucleate as a preventative measure against sympathetic ophthalmia. However, this procedure is extremely rare, and current reports indicate that only one soldier in OIF has undergone enucleation in a tertiary care facility to prevent sympathetic ophthalmia.

A contusion, commonly known as a bruise, is a type of hematoma of tissue in which capillaries and sometimes venules are damaged by trauma, allowing blood to seep, hemorrhage, or extravasate into the surrounding interstitial tissues. The bruise then remains visible until the blood is either absorbed by tissues or cleared by immune system action. Bruises, which do not blanch under pressure, can involve capillaries at the level of skin, subcutaneous tissue, muscle, or bone. Bruises are not to be confused with other similar-looking lesions primarily distinguished by their diameter or causation. These lesions include petechia (1 cm caused by blood dissecting through tissue planes and settled in an area remote from the site of trauma or pathology such as periorbital ecchymosis, e.g.,"raccoon eyes", arising from a basilar skull fracture or from a neuroblastoma).

As a type of hematoma, a bruise is always caused by internal bleeding into the interstitial tissues which does not break through the skin, usually initiated by blunt trauma, which causes damage through physical compression and deceleration forces. Trauma sufficient to cause bruising can occur from a wide variety of situations including accidents, falls, and surgeries. Disease states such as insufficient or malfunctioning platelets, other coagulation deficiencies, or vascular disorders, such as venous blockage associated with severe allergies can lead to the formation of purpura which is not to be confused with trauma-related bruising/contusion. If the trauma is sufficient to break the skin and allow blood to escape the interstitial tissues, the injury is not a bruise but instead a different variety of hemorrhage called bleeding. However, such injuries may be accompanied by bruising elsewhere.

Bruises often induce pain, but small bruises are not normally dangerous alone. Sometimes bruises can be serious, leading to other more life-threatening forms of hematoma, such as when associated with serious injuries, including fractures and more severe internal bleeding. The likelihood and severity of bruising depends on many factors, including type and healthiness of affected tissues. Minor bruises may be easily recognized in people with light skin color by characteristic blue or purple appearance (idiomatically described as "black and blue") in the days following the injury.

Aetiology of CTS is multifactorial, the causative factors include:

- previous restorative procedures.

- occlusal factors

- developmental conditions/anatomical considerations.

- trauma

- others, e.g, aging dentition or presence of lingual tongue studs.

Most commonly involved teeth are mandibular molars followed by maxillary premolars, maxillary molars and maxillary premolars. in a recent audit, mandibular first molar thought to be most affected by CTS possibly due to the wedging effect of opposing pointy, protruding maxillary mesio-palatal cusp onto the mandibular molar central fissure.

The presence of bruises may be seen in patients with platelet or coagulation disorders, or those who are being treated with an anticoagulant. Unexplained bruising may be a warning sign of child abuse, domestic abuse, or serious medical problems such as leukemia or meningoccocal infection. Unexplained bruising can also indicate internal bleeding or certain types of cancer. Long-term glucocorticoid therapy can cause easy bruising. Bruising present around the navel (belly button) with severe abdominal pain suggests acute pancreatitis. Connective tissue disorders such as Ehlers-Danlos syndrome may cause relatively easy or spontaneous bruising depending on the severity.

During an autopsy, bruises accompanying abrasions indicate the abrasions occurred while the individual was alive, as opposed to damage incurred post mortem.

Loss of attachment:

- By far the most common cause is periodontal disease (gum disease). This is painless, slowly progressing loss of bony support around teeth. It is made worse by smoking and the treatment is by improving the oral hygiene above and below the gumline.

- Dental abscesses can cause resorption of bone and consequent loss of attachment. Depending on the type of abscess, this loss of attachment may be restored once the abscess is treated, or it may be permanent.

- Many other conditions can cause permanent or temporary loss of attachment and increased tooth mobility. Examples include: Langerhans cell histiocytosis.

Increased forces on the tooth:

- Bruxism (abnormal clenching and grinding of teeth) can aggravate attachment loss and tooth mobility if periodontal disease is already present. The tooth mobility is typically reversible and the tooth returns to normal level of mobility once the bruxism is controlled.

- Dental trauma. Luxations, and root fractures of teeth can cause sudden mobility after a blow. Dental trauma may be isolated or associated with other facial trauma.

- Increased biting force on one tooth can cause temporary increased mobility until corrected. A common scenario is a new filling or crown which is a fraction of a millimeter too prominent in the bite, which after a few days causes periodontal pain in that tooth and/or the opposing tooth.

Cracked tooth syndrome (abbreviated to CTS, and also termed cracked cusp syndrome, split tooth syndrome, or incomplete fracture of posterior teeth), is where a tooth has incompletely cracked but no part of the tooth has yet broken off. Sometimes it is described as a greenstick fracture. The symptoms are very variable, making it a notoriously difficult condition to diagnose.

Due to the rarity of the condition, it's difficult to reliably estimate statistics. However, a 2006 study which followed 7 cases over an average of 8.5 years noted that "In general, cherubism does not have a poor prognosis. It has been noted that the condition does not progress beyond puberty. As the patient grows to adulthood, the jawbone lesions tend to resolve, and a progressively more normal jaw configuration is noted.".

Because this genetic anomaly is genetically linked, genetic counseling may be the only way to decrease occurrences of Cherubism. The lack of severe symptoms in the parents may be the cause of failure in recognizing the disorder. The optimal time to be tested for mutations is prior to having children. The disorder results from a genetic mutation, and this gene has been found to spontaneously mutate. Therefore, there may be no prevention techniques available.

It can be caused by any of the following:

- Nutritional factors.

- Some diseases (such as undiagnosed and untreated celiac disease, chicken pox, congenital syphilis).

- Hypocalcemia.

- Fluoride ingestion (dental fluorosis).

- Birth injury.

- Preterm birth.

- Infection.

- Trauma from a deciduous tooth.