Diseases of the teeth and the eye

A significant number of combined pathologies of the eye and organs of the dental system are known: neuralgia with pain radiating to the eye, vasomotor disorders accompanied by conjunctival hyperemia, hypo- and hypersecretion of lacrimal fluid and saliva, motor disorders affecting the motor apparatus of the eye, neurotrophic lesions of the dental system, cornea, sclera, uveal tract, retina, optic nerve, orbit.

Changes in the eye often occur with dental diseases such as caries, periodontitis, periostitis, abscesses, gangrene, periodontosis, granulomas. With dental fanulomas and chronic inflammation of the periodontium, the terminal ends of not only the trigeminal but also the sympathetic nerve are irritated, which causes a pathological reflex effect on the eye and other organs. Foci of pathological irritation can occur after the treatment of depulped, filled or covered with metal crowns teeth. There are known cases of development of accommodation paralysis of odontogenic origin.

The appearance of flickering, dark and light spots, stars, stripes or fog before the eyes, and decreased vision of varying duration can in some cases be explained by reflex vascular reactions originating from dental foci.

Teething can cause blepharospasm and conjunctival hyperemia.

Odontogenic infection can cause thrombophlebitis and inflammation of the facial veins, often on the side of the upper teeth affected by caries. Caries, periodontitis, abscesses, periostitis, osteomyelitis, periodontosis, fanulomas cause various changes in the eye. Sometimes the infection spreads to the adjacent paranasal cavities and then affects the eye.

The cause of such inflammatory diseases as orbital cellulitis, osteoperiostitis and subperiosteal orbital abscesses can also be erysipelas, furuncles and abscesses of the skin of the face and head, various inflammatory diseases of the dental system - acute and chronic pericementitis, periradicular fanulomas of the jaws, cellulitis and abscesses of the maxillofacial region and neck.

In infants, the most common cause of orbital cellulitis is inflammation of the maxilla. After hematogenous osteomyelitis of the maxilla, defects of the lower orbital margin with cicatricial eversion of the eyelids usually form.

Acute inflammation of the orbit should be differentiated from hematogenous osteomyelitis of the maxilla, chronic osteomyelitis of the maxilla - from dacryocystitis, abscesses of the infraorbital margin - from cellulitis of the lacrimal sac.

Malignant tumors of the paranasal sinuses, both primary and secondary (growing from the nasopharynx), tumors of the maxilla, hard and soft palate penetrate into the orbit. In this case, the ophthalmologist can detect the first symptoms: congestion is noted in the fundus as a result of compression of the optic nerve and blood vessels, exophthalmos and diplopia occur, and the earliest symptom is swelling of the eyelids. especially in the morning. With tumors originating from the main sinus, persistent headache, axial exophthalmos, decreased visual acuity are noted, in the fundus - congestion of the optic nerve.

The development of combined orbital and maxillofacial tumors is possible. Hemangiomas, lymphangiomas, and dermoids are most often detected. These tumors can be located under the muscles of the floor of the mouth, under the tongue, in the tongue, and in the root of the nose.

Congenital cleft lip and palate, enamel hypoplasia may be combined with congenital cataracts. Against the background of tetany, layered cataracts and layered distribution of enamel in teeth often occur.

Bilateral, often significantly pronounced exophthalmos can be caused by underdevelopment of the upper jaw and orbit. In craniofacial exostoses, a Mongoloid facial type, astigmatism, nystagmus, subluxation of the lens, deformation of the skull, open bite, cranial nerve palsy, etc. can be observed.

Behcet's disease. Turkish dermatologist H. Behcet (1937) combined recurrent hypopyon-iridocyclitis, aphthous stomatitis, ulceration of the genitals and skin lesions into one syndrome.

Men get sick more often and mainly at the age of 20-30 years. Very rarely the disease can begin in childhood.

The disease occurs suddenly, occurs in attacks that last from several weeks to several months and then recur over a long period of time - up to 25 years. During the year, as a rule, there are 4-5 exacerbations, both eyes are affected, sometimes simultaneously, more often at different times.

The presence of all symptoms is observed in approximately '/ ₃ of patients, more often individual symptoms appear at intervals of several months or even years. This complicates timely diagnosis.

The duration of the incubation period is not established. The disease rarely begins with eye symptoms, more often with malaise and fever, the appearance of aphthae on the mucous membrane of the oral cavity and tongue, then ulceration of the genitals occurs.

Aphthae are painful and look like whitish-yellowish spots surrounded by a red rim of varying size. More often, several aphthae are formed, and very rarely - single ones. Aphthae disappear without leaving a trace.

Aphthous stomatitis most often coincides with an exacerbation of hypopyon-iridocyclitis. Ulcerations of the genitals are manifested by small superficial ulcers, the formation of papules or vesicles, which then ulcerate. After their disappearance, pigmentation or scars remain. Hypopyon-iridocyclitis develops at different times from the onset of the disease, which is more severe with each relapse. Patients note a decrease in vision, the fluid of the anterior chamber becomes cloudy, then hypopyon, the iris becomes hyperemic, opacities of varying intensity form in the vitreous body. Hypopyon initially resolves quite quickly, as do opacities of the vitreous body. As a result of repeated attacks, posterior synechiae are formed, exudate is organized in the pupil area, intraocular pressure increases, complicated cataracts and persistent opacities of the vitreous body develop. The process, as a rule, ends in blindness.

The disease sometimes begins with exudative chorioretinitis, neuroretinitis, periarteritis with hemorrhages in the retina and vitreous body, retrobulbar neuritis, papillitis, optic nerve atrophy, and degenerative changes in the retina. The results of fluorescence angiography indicate that Behcet's disease involves generalized damage to the vascular system of the eye.

Pathological changes in the fundus are a factor that determines a poor prognosis for vision in Behcet's disease.

In rare cases, the disease is accompanied by conjunctivitis and superficial keratitis with recurrent corneal ulcerations or the presence of stromal infiltrates.

Skin lesions manifest as folliculitis, furuncles, erythema nodosum, erosive ectoderma, and pyoderma.

Other symptoms are also described: tracheobronchitis, thrombophlebitis and thrombosis of the veins of the lower extremities, joint diseases such as rheumatoid polyarthritis, tonsillitis, orchitis, damage to the nervous system in the form of meningoencephalitis.

It should be noted that pain and swelling in the affected joints, i.e. arthropathies, can be the first symptom of Behcet's disease.

Diagnosis is based on a complex of clinical signs.

Behcet's disease is differentiated from sarcoidosis, encephalitis, Crohn's disease, Reiter's and Stevens-Johnson syndromes and other diseases with similar clinical presentations.

There is no effective treatment, nor is there a generally accepted system of treatment.

The treatment used - broad-spectrum antibiotics, sulfonamides, calcium chloride, transfusion of the same blood group, plasma in fractional doses, globulin, corticosteroids under the conjunctiva retrobulbarly and orally, atropine instillation, autohemotherapy, ultrasound and dehydration therapy, etc. - provides only temporary improvement.

Currently, treatment is supplemented with immunosuppressants and immunomodulators.

Sjogren's syndrome. The clinical symptoms of the disease are lesions of the lacrimal and salivary glands, upper respiratory tract and gastrointestinal tract, arising against the background of deforming polyarthritis. The disease develops slowly, the course is chronic with exacerbations and remissions.

Patients' complaints are limited to a feeling of pain, dryness, burning in the eyes, difficulty opening the eyes in the morning, photophobia, fogging, lack of tears when crying, deterioration of vision and pain in the eye. An objective examination may reveal slight hyperemia and looseness of the conjunctiva of the eyelids, viscous discharge from the conjunctival cavity in the form of thin grayish elastic threads (mucus and exfoliated epithelial cells).

The cornea loses its shine and becomes thinner. There are grayish threads on its surface, after removal of which erosions may remain, and subsequently its opacity develops with ingrowth of vessels, the process ends with xerosis. The sensitivity of the cornea does not change. Using Schirmer's test No. 1, a decrease in the function of the lacrimal glands is detected (from 3-5 mm to 0).

After some time, after the appearance of eye pathology, changes in the mucous membrane of the oral cavity and tongue are noted. Saliva becomes viscous, as a result of which speech, chewing and swallowing are difficult. Food has to be washed down with water. After some time, dryness develops due to lack of saliva (sialopenia), and later, a drop of thick yellowish saliva can be squeezed out of the opening of the Stenon duct (parotid gland duct) with great difficulty. Later, the parotid salivary glands enlarge, which is sometimes mistakenly regarded as a sign of epidemic parotitis. The mucous membrane of the oral cavity and the red border of the lips become dry, erosions and cracks appear on the tongue. Dryness spreads to the mucous membrane of the pharynx, esophagus, stomach, larynx, trachea, etc., since the nasopharyngeal, buccal, gastric, tracheobronchial and other glands are involved in the process. Gastritis and colitis develop, hoarseness and sometimes a dry cough appear. Less often, the mucous membrane of the urethra, rectum and anus is affected.

As a result of decreased secretion of sweat and sebaceous glands, dry skin appears, hyperkeratosis, hyperpigmentation, and hair loss may be observed.

Most patients experience arthropathies in the form of chronic deforming polyarthritis, subfebrile temperature, increased ESR, normo- and hypochromic anemia, first leukocytosis, then leukopenia, albuminoglobulin shift, liver dysfunction, disorders in the cardiovascular and genitourinary systems, and neurological disorders.

Not all symptoms occur simultaneously, but dryness of the conjunctiva and cornea, mucous membrane of the oral cavity and nose are constant signs of this syndrome. The course of the disease is chronic. Both eyes are always affected.

According to modern concepts, the disease is related to collagenoses, a group of autoimmune diseases. For diagnostics, the following procedure for conducting studies of the function of the salivary glands is proposed: cytological examination of smears of secretion, radiosialography, radiometric examination of saliva, scanning, contrast radiographic examination of the glands and a complete ophthalmological examination with a study of the functional state of the lacrimal glands.

Treatment is symptomatic: vitamin therapy, immunosuppressants, oral drops of 5% pilocarpine solution, subcutaneous injections of 0.5% galantamine solution, local instillation of artificial tears, corticosteroids, lysozyme, peach and sea buckthorn oil, laser stimulation of the parotid salivary and lacrimal glands.

Stevens-Johnson syndrome. Characteristic signs of the disease are erosive inflammation of the mucous membranes of most natural openings, polymorphic rashes on the skin, fever. The dominant symptom is damage to the mucous membranes of the oral cavity, nasopharynx, eyes and genitals.

The disease is more often observed in children and adolescents, but can occur at any age. Relapses occur in spring and autumn. The disease is associated with focal infection, drug allergy, autoimmune processes. It most often begins with the appearance of headache, malaise and chills, an increase in body temperature to 38-39 ° C, depression or irritability, joint pain. Subsequently, a polymorphic rash appears on the skin of the face, trunk, limbs. This is preceded by severe lesions of the mucous membranes of the oral cavity, nasopharynx, eyes and genitals. On the mucous membranes of the cheeks, gums, tonsils, pharynx, palate, tongue and lips, there is a sharply expressed hyperemia and edema with the formation of quickly bursting blisters. The blisters, merging, turn into continuous bleeding erosions. The tongue enlarges and becomes covered with a mucopurulent coating, which causes severe pain, salivation, and difficulty speaking and eating. The lymph nodes are enlarged, especially the cervical ones.

Eye diseases are observed in all patients. Conjunctival lesions manifest themselves in the form of catarrhal, purulent or membranous conjunctivitis. The eyelids are edematous, hyperemic, glued together with abundant purulent-bloody exudate. Catarrhal conjunctivitis ends well, leaving no consequences. In purulent conjunctivitis, due to the addition of a secondary infection, the cornea is involved in the process, superficial or deep ulceration occurs with subsequent scarring, and sometimes perforation, resulting in partial or complete blindness. Membranous conjunctivitis is accompanied by conjunctival necrosis and ends in scarring. The consequences are trichiasis, eversion of the eyelids, xerosis, symblepharon and even ankyloblepharon. Ocular manifestations of this syndrome are not limited to conjunctivitis. Cases of iritis, episcleritis, dacryocystitis and even panophthalmitis have also been described.

Patients are mistakenly diagnosed with measles, foot-and-mouth disease, trachoma, diphtheria of the eye, pemphigus, and smallpox.

Treatment - broad-spectrum antibiotics in combination with sulfonamides, vitamins, corticosteroids, desensitizing agents, blood transfusions, immune serum. Locally, corticosteroids are used in the form of drops and subconjunctival injections, vitamin drops, and artificial tears in case of dryness. Surgical treatment is indicated for trichiasis, eversion, and xerosis.

Nasociliary nerve syndrome (Charlin syndrome) is a complex of symptoms caused by neuralgia of the nasociliary nerve, the largest branch of the first branch of the trigeminal nerve. Long ciliary nerves extend from it to the eyeball.

When the nasociliary nerve is irritated in the area of its innervation, changes in sensitivity (pain), impaired secretion (lacrimation, increased secretory function of the mucous membrane of the nasal cavity) and trophic disorders (in the skin and cornea) are observed.

The disease is associated with hypertrophy of the middle nasal concha, curvature of the nasal septum, adenoids in the nasopharynx, polyps, sinusitis, and facial trauma.

The syndrome manifests itself with sudden attacks of acute pain in the eye, around it, the corresponding half of the head, blepharospasm, lacrimation, pain and abundant secretion from the nostril on the affected side. An attack of pain can last from 10-60 minutes to several days and even weeks. If the cause of neuralgia is not eliminated, then superficial, ulcerative or neurotrophic keratitis, iritis or iridocyclitis develop.

Treatment consists of eliminating the underlying cause of the disease. Subjective sensations are temporarily relieved by lubricating the nasal mucosa with a 5% solution of cocaine with adrenaline. Antibiotics, tranquilizers, painkillers, sleeping pills, and ganglionic blockers are used.

The syndrome should be differentiated from lesions of the pterygopalatine ganglion and other facial neuralgias.

Sphenopalatine ganglion syndrome (Sluder's syndrome) is a complex of symptoms caused by neuralgia of the pterygopalatine ganglion.

The pterygopalatine ganglion is a formation of the parasympathetic nervous system. It contains multipolar cells and has three roots: sensory, parasympathetic and sympathetic. The branches of the pterygopalatine ganglion innervate the lacrimal gland, the mucous membrane of the palate, the mucous membrane of the nose, the posterior cells of the ethmoid bone and the sinuses of the maxillary and sphenoid bones.

At the onset of the disease, the patient experiences sharp shooting pains at the base of the nose, around and behind the eye, in the eye, in the upper and lower jaw, in the teeth. The pain radiates to the temple, ear, neck, shoulder, forearm and hand. The most intense pain is in the orbit, root of the nose and mastoid process. The pain lasts from several hours and days to several weeks.

During an attack, the patient also complains of a burning sensation in the nose, sneezing attacks, runny nose, lacrimation, salivation, dizziness, nausea, and there may be asthma-like attacks and taste perversion.

From the side of the eyes, there is a sharp photophobia, blepharospasm, lacrimation, there may be swelling of the upper eyelid, conjunctival hyperemia, mydriasis or miosis, sometimes a short-term increase in intraocular pressure (IOP). The disease can last for a long time, sometimes for months and even years. In the interictal period, a dull pain in the upper jaw, root of the nose, eye socket often remains, and swelling of the affected half of the face may remain.

Neuralgia of the pterygopalatine ganglion is associated with perifocal infection of the paranasal sinuses and oral cavity, infection in various parts of the head (purulent otitis, cerebral arachnoiditis), with nasal trauma, hypertrophy of the turbinates and curvature of the nasal septum, peritonsillar abscesses, and allergies.

The cause may also be retromaxillary tumors.

Unlike the nasociliary nerve syndrome, when the pterygopalatine ganglion is affected, there are no anatomical changes in the anterior segment of the eyeball. Increased sensitivity of the nasal mucosa is concentrated in the posterior part of the nasal cavity. It is necessary to differentiate it from other facial neuralgias.

During an attack, a cocaine block in the area of the pterygopalatine ganglion is recommended. Treatment should be aimed primarily at eliminating the underlying cause of the disease.

Prescribed are painkillers and decongestants, corticosteroids, anti-infective therapy, ganglionic blockers, anticholinergic agents and physiotherapeutic procedures, biogenic stimulants.

Ciliary ganglion syndrome (Hageman-Pochtman syndrome) occurs when the ciliary ganglion, located behind the eyeball (12-20 mm) between the beginning of the external rectus muscle and the optic nerve, becomes inflamed. 4-6 short ciliary nerves extend from the ciliary ganglion to the eye.

The disease manifests itself with sudden pains in the head and deep in the orbit, radiating to the jaws and teeth. The pains may intensify with movement of the eyeball and pressure on it. They may radiate to the corresponding half of the head. The pains last from several days to several weeks.

Patients have unilateral mydriasis with preservation of the correct round shape of the pupil, absence of pupillary reactions to light and convergence, weakness or paralysis of accommodation, corneal hypoesthesia, possible edema of the epithelium and transient increase in ophthalmotonus. Optic neuritis rarely develops. The syndrome is usually unilateral. It usually passes in 2-3 days, sometimes in a week or later. Paralysis or paresis of accommodation persists the longest, which is sometimes the only evidence of the process suffered. Relapses are possible.

The causes of the disease are inflammatory processes in the paranasal sinuses, teeth, infectious diseases, trauma or contusion of the orbit.

Treatment: sanitation of the paranasal sinuses, oral cavity, ganglionic blockades, corticosteroids, vitamin and pyrotherapy, diphenhydramine, novocaine retrobulbar, locally - quinine with morphine, vitamin drops.

Marcus-Gun syndrome. Paradoxical eyelid movements - unilateral ptosis, disappearing when opening the mouth and moving the jaw in the opposite direction. If the mouth opens more, the palpebral fissure may become wider. When chewing, ptosis decreases. The syndrome can be congenital and acquired, more often observed in men. With age, it may become less pronounced.

In acquired disease, paradoxical eyelid movements appear after trauma, tooth extraction, facial nerve injury, concussion, encephalitis, mental trauma. It is assumed that there is an abnormal connection between the trigeminal and oculomotor nerves or nuclei of these nerves. Sometimes this syndrome is considered as a result of a violation of corticobulbar connections.

There are associated changes in the visual organ and the body as a whole (paralytic strabismus on the side of ptosis, epilepsy with rare seizures, etc.). Treatment is mainly surgical - elimination of ptosis.

Martin Ama syndrome is a syndrome opposite to Marcus-Gun syndrome - drooping of the upper eyelid when opening the mouth. Ptosis also appears during chewing. The development of paradoxical synkinetic movements is preceded by peripheral paralysis of the facial nerve.

Mikulicz's disease is a symptom complex characterized by slowly progressing symmetrical, often significant enlargement of the lacrimal and salivary glands, downward and inward displacement of the eyeballs and their forward protrusion. Eye movements are limited, diplopia is sometimes present. The skin of the eyelids is stretched, may be cyanotic, dilated veins are visible in it, and hemorrhages are noted in the thickness of the eyelids. The conjunctiva of the eyelids is hyperemic. Perivasculitis, hemorrhages, signs of stagnant disk or neuritis are sometimes found in the fundus. The disease develops slowly, over several years. It usually begins at the age of 20-30 with gradually increasing swelling of the salivary, and then lacrimal glands, sometimes the process spreads even to the small glands of the oral cavity and larynx. The swollen large glands are mobile, elastic, painless, with a smooth surface. Suppuration of the glands never occurs. The lymph nodes are involved in the process. Pathological changes manifest themselves as lymphomatosis, less often granulomatosis of the lacrimal and salivary glands. Treatment depends on the suspected etiology of the disease. In all cases, the use of arsenic and potassium iodide solution orally is indicated.

The disease is differentiated from chronic productive parenchymatous inflammation of the salivary gland, salivary stone disease, tumors of the salivary and lacrimal glands, and Sjögren's syndrome.

Sturge-Beber-Krabbe syndrome is an encephalotrigeminal syndrome characterized by a combination of cutaneous and cerebral angiomatosis with ocular manifestations. Etiology is congenital neuroectodermal dysplasia. Cutaneous angiomatosis may be congenital or develop in early childhood in the form of facial angiomas, most often located on one half of the face along the first and second branches of the trigeminal nerve. The color of the lesions in infancy is pink, then becomes bluish-red. Angiomatosis of the facial skin often spreads to the skin of the eyelids, conjunctiva and sclera. Angioma can develop in the choroid, sometimes retinal detachment occurs according to the localization of the angioma. As a rule, the syndrome is accompanied by glaucoma, which occurs with minor hydrophthalmos. Symptoms of brain damage manifest as mental retardation, clonic seizures, epileptiform attacks, recurrent hemiparesis or hemiplegia. Hemangiomas in internal organs are possible. Endocrine disorders are also noted: acromegaly, obesity.

Treatment: X-ray therapy, sclerotherapy, surgical treatment of skin angiomas, treatment of glaucoma.

The prognosis for life is usually unfavorable due to severe neurological complications.

Craniofacial dysostosis (Crouzon's disease). The main symptom is bilateral, often significant exophthalmos, caused by underdevelopment of the maxilla and orbit.

Also observed are divergent strabismus, widening of the nasal root area, hypertelorism. In the fundus, there are congested optic discs with subsequent secondary atrophy as a result of narrowing of the optic canal or increased intracranial pressure due to synostosis of most cranial sutures. Mongoloid type of eye slits, astigmatism, nystagmus are observed, congenital subluxations of the lens, hydrophthalmos, cataracts may be noted. Other symptoms include tower-type skull deformation, beak-shaped nose, short upper lip, epileptic seizures, olfactory and auditory disorders, moderate mental retardation. Crouzon's disease is sometimes combined with open bite, syndactyly of the hands and feet.

The disease is considered a familial hereditary anomaly of the skull. Treatment is surgical bone grafting.

Mandibulofacial dysostosis (Franceschetti's disease) is a familial and hereditary syndrome characterized by a variety of maxillofacial anomalies in various combinations. In terms of the eyes, there are slanting "anti-Mongoloid" palpebral fissures (bilateral drooping of the outer corner of the palpebral fissure), colobomas of the eyelids, epibulbar dermoids, paresis of the extraocular muscles, rarely microphthalmos, congenital cataracts, colobomas of the vascular tract, and optic nerve.

On the part of the maxillofacial system, there is hypoplasia of the facial bones, which leads to significant facial asymmetry and severe underdevelopment of the teeth.

Often there is aplasia of the ears, hyperplasia of the frontal sinuses, splitting of the facial bones and deformation of the skeleton. Sometimes there is an enlarged tongue, absence of the parotid gland, hydrocephalus, heart damage, etc. Along with typical forms of the syndrome, there are also atypical ones, in which only some of the symptoms are present.

Meyer-Schwickerath-Grueterich-Weyers syndrome (ocolodentodigital dysplasia) - combined lesions of the eyes, face, teeth, fingers, hands, feet. Eye symptoms - epicanthus, narrow palpebral fissures, ptosis, bilateral microphthalmia, iris anomaly in the form of hypoplasia of the anterior leaflet, congenital glaucoma. From the dental side - generalized enamel dysplasia with brown coloring of microdontia and oligodontia. The face has a small nose, hypoplasia of the wings of the nose and a wide bridge of the nose. Of the limb anomalies, it is necessary to note a change in the skin between the fingers, a square appearance of the middle phalanx of the little finger, hypoplasia or complete absence of the middle phalanges of several fingers, dystrophy of the nails or their absence. Microcephaly, changes in the nose, hypotrichosis and insufficiency of skin pigmentation may also occur.

Rieger's syndrome is a hereditary ectomesodermal dysgenesis of the iris and cornea, combined with dentofacial changes. From the ocular side, there may be megalocornea or microcornea, flat cornea, remnants of mesenchymal tissue in the angle of the anterior chamber, marginal adhesions of the posterior surface of the cornea with the anterior surface of the iris, pupil deformation, iris atrophy with the formation of through defects, glaucoma. Congenital cataract, coloboma of the iris and choroid, strabismus, dermoid cysts at the limbus, high-degree refractive errors are possible.

Common manifestations include a wide nasal bridge, hypoplasia of the upper jaw, cleft palate, oligodontia, conical shape of the front teeth, dysplasia of dental enamel, hydrocephalus, malformations of the heart, kidneys, and spine. Some patients have short stature due to growth hormone deficiency.

The inheritance type is autosomal dominant.

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